1
40
68
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/j.1600-0714.1991.tb00428.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1600-0714.1991.tb00428.x</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
245-249
Issue
5
Volume
20
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
ULTRASTRUCTURAL CHARACTERISTICS OF A CELL-LINE DERIVED FROM A MELANOTIC NEUROECTODERMAL TUMOR OF INFANCY
Publisher
An entity responsible for making the resource available
Journal of Oral Pathology & Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
1991
1991-05
Subject
The topic of the resource
Pathology; cell line; Dentistry; Oral Surgery & Medicine; freeze-fracture; melanotic neuroectodermal tumor of infancy; transmission electron microscopy
Creator
An entity primarily responsible for making the resource
Claman L J; Stetson D; Steinberg B; Shuler C F
Description
An account of the resource
Thin section and freeze-fracture transmission electron microscopy were used to examine and identify the cytoplasmic and membrane structures in a cell line derived from a melanotic neuroectodermal tumor of infancy (MNTI). The cultured cells had a uniform appearance after 70 population doublings characterized by long dendritic processes and evidence of melanin production. The cytoplasm contained numerous melanosomes in various stages of development, vesiculated rough endoplasmic reticulum, microfilaments and uncoated as well as coated vesicles. The membrane specializations included caveoli, coated pits, gap junctions, microfilaments, desmosome-like structures and lamellipodia. The ultrastructural appearance of the cultured MNTI cells was similar to features previously seen in electron micrographs of MNTI tumor specimens. However, correlated freeze-fracture and thin section micrographs permitted further identification of structures previously described. The MNTI cell line represents one of the cell types of the tumor and provides an opportunity for further study of the pathogenesis of this rare tumor.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1600-0714.1991.tb00428.x" target="_blank" rel="noreferrer noopener">10.1111/j.1600-0714.1991.tb00428.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1991
Cell Line
Claman L J
Dentistry
freeze-fracture
Journal Article or Conference Abstract Publication
Journal of Oral Pathology & Medicine
melanotic neuroectodermal tumor of infancy
Oral Surgery & Medicine
Pathology
Shuler C F
Steinberg B
Stetson D
transmission electron microscopy
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jnr.21035" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jnr.21035</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1303-1310
Issue
6
Volume
84
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of Down syndrome
Publisher
An entity responsible for making the resource available
Journal of Neuroscience Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-11
Subject
The topic of the resource
16 mice; abnormalities; acetylcholine; acetylcholine-release; alzheimers-disease; amyloid; antisense; beta-protein; calcium; cell line; Down syndrome; Neurosciences & Neurology; neurotoxicity; peptide; rat hippocampal slices; root ganglion neurons
Creator
An entity primarily responsible for making the resource
Opazo P; Saud K; de Saint Pierre M; Cardenas A M; Allen D D; Segura-Aguilar J; Caviedes R; Caviedes P
Description
An account of the resource
We have generated immortal neuronal cell lines from normal and trisomy 16 (Ts16) mice, a model for Down syndrome (DS). Ts16 lines overexpress DS-related genes (App, amyloid precursor protein; Sod1, Cu/Zn superoxide dismutase) and show altered cholinergic function (reduced choline uptake, ChAT expression and fractional choline release after stimulation). As previous evidence has related amyloid to cholinergic dysfunction, we reduced APP expression using specific mRNA antisense sequences in our neuronal cell line named CTb, derived from Ts16 cerebral cortex, compared to a cell line derived from a normal animal, named CNh. After transfection, Western blot studies showed APP expression knockdown in CTb cells of 36% (24 hr), 40.4% (48 hr), and 50.2% (72 hr) compared to CNh. Under these reduced APP levels, we studied 3 H-choline uptake in CTb and CNh cells. CTb, as reported previously, expressed reduced choline uptake compared to CNh cells (75%, 90%, and 69% reduction at 1, 2, and 5 min incubation, respectively). At 72 hr of APP knockdown, choline uptake levels were essentially similar in both cell types. Further, fractional release of H-3-choline in response to glutamate, nicotine, and depolarization with KCI showed a progressive increase after APP knockdown, reaching values similar to those of CNh after 72 hr of transfection. The results suggest that APP overexpression in CTb cells contributes to impaired cholinergic function, and that gene knockdown in CTb cells is a relevant tool to study DS-related dysfunction. (c) 2006 Wiley-Liss, Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jnr.21035" target="_blank" rel="noreferrer noopener">10.1002/jnr.21035</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
16 mice
2006
Abnormalities
Acetylcholine
acetylcholine-release
Allen D D
alzheimers-disease
amyloid
antisense
beta-protein
calcium
Cardenas A M
Caviedes P
Caviedes R
Cell Line
de Saint Pierre M
Down syndrome
Journal Article
Journal of neuroscience research
Neurosciences & Neurology
Neurotoxicity
Opazo P
peptide
rat hippocampal slices
root ganglion neurons
Saud K
Segura-Aguilar J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
191–197
Issue
1
Volume
272
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Transcriptional regulation of human oxysterol 7 alpha-hydroxylase gene (CYP7B1) by Sp1.
Publisher
An entity responsible for making the resource available
Gene
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-07
Subject
The topic of the resource
Humans; Protein Binding; Gene Expression Regulation; Cell Line; Transfection; Base Sequence; Binding Sites/genetics; Molecular Sequence Data; Cytochrome P450 Family 7; Mutagenesis; Luciferases/genetics/metabolism; Recombinant Fusion Proteins/genetics/metabolism; CpG Islands/genetics; Cytochrome P-450 Enzyme System/*genetics/metabolism; DNA/genetics; Sequence Deletion; Sp1 Transcription Factor/metabolism/*physiology; Steroid Hydroxylases/*genetics/metabolism; Cultured; Binding; Competitive; Transcription; Genetic; Enzymologic; Tumor Cells; Site-Directed; Regulatory Sequences; Nucleic Acid/genetics
Creator
An entity primarily responsible for making the resource
Wu Z; Chiang J Y
Description
An account of the resource
Oxysterol 7 alpha-hydroxylase catalyzes hydroxylation of oxysterols and neurosterols and plays a role in the alternative bile acid synthesis pathway. This gene is widely expressed in many organs and peripheral tissues and may protect tissues from the toxicity of oxysterols. Mutation in CYP7B1 caused neonatal cholestasis. To examine the regulatory mechanisms governing CYP7B1 expression, the 5' flanking sequence of the CYP7B1 was analyzed and revealed a CpG island of about 1.2 kb. Transient transfection assays of deletion mutants of the CYP7B1 promoter-luciferase reporter gene in human liver-derived HepG2, fibroblast NT1088, and human embryonic kidney 293 cell lines revealed that the region from -291 to +189 was critical for gene transcription. Three GC box sequences located between -25 and +10 were essential for basal transcription because mutations of these sequences markedly reduced promoter activity. Sp1 and Sp3 bound to these sequences as demonstrated by DNase I footprinting assays and electrophoretic mobility shift assay. Thus, regulation of CYP7B1 transcription by Sp1 may play a pivotal role in regulating oxysterol levels, which regulate cholesterol metabolism.
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2001
Base Sequence
Binding
Binding Sites/genetics
Cell Line
Chiang J Y
Competitive
CpG Islands/genetics
Cultured
Cytochrome P-450 Enzyme System/*genetics/metabolism
Cytochrome P450 Family 7
Department of Integrative Medical Sciences
DNA/genetics
Enzymologic
gene
Gene Expression Regulation
Genetic
Humans
Luciferases/genetics/metabolism
Molecular Sequence Data
Mutagenesis
NEOMED College of Medicine
Nucleic Acid/genetics
Protein Binding
Recombinant Fusion Proteins/genetics/metabolism
Regulatory Sequences
Sequence Deletion
Site-Directed
Sp1 Transcription Factor/metabolism/*physiology
Steroid Hydroxylases/*genetics/metabolism
Transcription
Transfection
Tumor Cells
Wu Z
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
2195–2203
Issue
12
Volume
40
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Structure and functions of human oxysterol 7alpha-hydroxylase cDNAs and gene CYP7B1.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-12
Subject
The topic of the resource
Humans; Animals; Mice; Cell Line; Transfection; Base Sequence; Molecular Sequence Data; Chromosome Mapping; Cytochrome P450 Family 7; DNA; Luciferases/genetics; Cytochrome P-450 Enzyme System/*genetics/metabolism; Steroid Hydroxylases/*genetics/metabolism; Hydroxycholesterols/metabolism; Codon; Northern; Blotting; Transcription; Genetic; Cloning; Molecular; Genetic/genetics; Promoter Regions; Nucleic Acid; Complementary/biosynthesis/*isolation & purification; Initiator; Regulatory Sequences
Creator
An entity primarily responsible for making the resource
Wu Z; Martin K O; Javitt N B; Chiang J Y
Description
An account of the resource
Oxysterol 7alpha-hydroxylase has broad substrate specificity for sterol metabolites and may be involved in many metabolic processes including bile acid synthesis and neurosteroid metabolism. The cloned human oxysterol 7alpha-hydroxylase (CYP7B1) cDNA encodes a polypeptide of 506 amino acid residues that shares 40% sequence identity to human cholesterol 7alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver. In contrast to the liver-specific expression of CYP7A1, CYP7B1 mRNA transcripts were detected in human tissues involved in steroid genesis (brain, testes, ovary, and prostate) and in bile acid synthesis (liver) and reabsorption (colon, kidney, and small intestine). The human oxysterol 7alpha-hydroxylase transiently expressed in 293/T cells was able to catalyze 7alpha-hydroxylation of
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1999
Animals
Base Sequence
Blotting
Cell Line
Chiang J Y
Chromosome Mapping
Cloning
Codon
Complementary/biosynthesis/*isolation & purification
Cytochrome P-450 Enzyme System/*genetics/metabolism
Cytochrome P450 Family 7
Department of Integrative Medical Sciences
DNA
Genetic
Genetic/genetics
Humans
Hydroxycholesterols/metabolism
Initiator
Javitt N B
Journal of lipid research
Luciferases/genetics
Martin K O
Mice
Molecular
Molecular Sequence Data
NEOMED College of Medicine
Northern
Nucleic Acid
Promoter Regions
Regulatory Sequences
Steroid Hydroxylases/*genetics/metabolism
Transcription
Transfection
Wu Z
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
1831–1841
Issue
9
Volume
37
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Transcriptional regulation of the human cholesterol 7 alpha-hydroxylase gene (CYP7A) in HepG2 cells.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
1996
1996-09
Subject
The topic of the resource
Humans; Binding Sites; Gene Expression Regulation; Cell Line; Transfection; Base Sequence; Molecular Sequence Data; Phorbol Esters/pharmacology; DNA-Binding Proteins/genetics/metabolism; *Transcription Factors; Enzyme Repression; Cholesterol 7-alpha-Hydroxylase/biosynthesis/*genetics; Consensus Sequence; Glucocorticoids/pharmacology; Hepatocyte Nuclear Factor 3-alpha; Insulin/pharmacology; Nuclear Proteins/genetics/metabolism; Recombinant Fusion Proteins/biosynthesis; Thyroid Hormones/pharmacology; Genes; Receptors; Enzymologic/*drug effects; Genetic; *Promoter Regions; Reporter; *Transcription; Glucocorticoid/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Wang D P; Stroup D; Marrapodi M; Crestani M; Galli G; Chiang J Y
Description
An account of the resource
A stable HepG2 cell line harboring a human cholesterol 7 alpha-hydroxylase (CYP7A) minigene/luciferase reporter gene construct was selected for studying transcriptional regulation of CYP7A gene promoter. Insulin and phorbol
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Promoter Regions
*Transcription
*Transcription Factors
1996
Base Sequence
Binding Sites
Cell Line
Chiang J Y
Cholesterol 7-alpha-Hydroxylase/biosynthesis/*genetics
Consensus Sequence
Crestani M
Department of Integrative Medical Sciences
DNA-Binding Proteins/genetics/metabolism
Enzyme Repression
Enzymologic/*drug effects
Galli G
Gene Expression Regulation
Genes
Genetic
Glucocorticoid/genetics/metabolism
Glucocorticoids/pharmacology
Hepatocyte Nuclear Factor 3-alpha
Humans
Insulin/pharmacology
Journal of lipid research
Marrapodi M
Molecular Sequence Data
NEOMED College of Medicine
Nuclear Proteins/genetics/metabolism
Phorbol Esters/pharmacology
Receptors
Recombinant Fusion Proteins/biosynthesis
Reporter
Stroup D
Thyroid Hormones/pharmacology
Transfection
Wang D P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
191–208
Issue
2
Volume
1
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Natural cytotoxins in human plasma: isolation and characterization of phospholipids associated with cytotoxic lipoproteins.
Publisher
An entity responsible for making the resource available
Molecular toxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
1987
1987-09
Subject
The topic of the resource
Animals; Mice; Cell Line; Chromatography; Cytotoxins/*blood; Lipoproteins/*blood; Molecular Weight; Phospholipids/*blood; Type C Phospholipases/pharmacology; Ultracentrifugation; Thin Layer
Creator
An entity primarily responsible for making the resource
Prezioso J A; Koo P H
Description
An account of the resource
Most of the heat-stable natural cytotoxins in normal human plasma were fractionated by gel filtration into two active fractions: the alpha
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1987
Animals
Cell Line
Chromatography
Cytotoxins/*blood
Koo P H
Lipoproteins/*blood
Mice
Molecular toxicology
Molecular Weight
Phospholipids/*blood
Prezioso J A
Thin Layer
Type C Phospholipases/pharmacology
Ultracentrifugation
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
191–195
Issue
1
Volume
304
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Guggulsterone antagonizes farnesoid X receptor induction of bile salt export pump but activates pregnane X receptor to inhibit cholesterol 7alpha-hydroxylase gene.
Publisher
An entity responsible for making the resource available
Biochemical and biophysical research communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
2003-04
Subject
The topic of the resource
Humans; Cell Line; Gene Expression Regulation/drug effects; Pregnane X Receptor; Cholesterol 7-alpha-Hydroxylase/*genetics; ATP-Binding Cassette Transporters/*genetics; Chenodeoxycholic Acid/antagonists & inhibitors; DNA-Binding Proteins/*antagonists & inhibitors/metabolism; Pregnenediones/*pharmacology; Transcription Factors/*antagonists & inhibitors/metabolism; Transcriptional Activation/drug effects; Dose-Response Relationship; Drug; Receptors; ATP Binding Cassette Transporter; Subfamily B; Cytoplasmic and Nuclear/*metabolism; Steroid/*metabolism; Member 11
Creator
An entity primarily responsible for making the resource
Owsley Erika; Chiang John Y L
Description
An account of the resource
Bile acids activate a nuclear receptor, farnesoid X receptor (FXR), that induces bile salt export pump (BSEP) but inhibits cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription in the liver. Guggulsterone, a plant sterol that lowers serum cholesterol, has been shown to antagonize FXR activated genes. Transient transfection assay of a human BSEP/luciferase reporter in HepG2 cells transfected with FXR reveals that guggulsterone strongly antagonizes bile acid induction of the BSEP gene. On the other hand, guggulsterone has no effect on FXR inhibition of the CYP7A1 gene, but strongly inhibits the human CYP7A1 gene by activation of pregnane X receptor (PXR). These results suggest that guggulsterone inhibits bile acid secretion from hepatocytes into bile and activates PXR to inhibit bile acid synthesis in the liver. Reduced conversion of cholesterol and bile acid excretion may lead to an increase of hepatic cholesterol and decrease of intestinal cholesterol absorption, and results in lowering serum cholesterol.
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2003
ATP Binding Cassette Transporter
ATP-Binding Cassette Transporters/*genetics
Biochemical and biophysical research communications
Cell Line
Chenodeoxycholic Acid/antagonists & inhibitors
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics
Cytoplasmic and Nuclear/*metabolism
Department of Integrative Medical Sciences
DNA-Binding Proteins/*antagonists & inhibitors/metabolism
Dose-Response Relationship
Drug
Gene Expression Regulation/drug effects
Humans
Member 11
NEOMED College of Medicine
Owsley Erika
Pregnane X Receptor
Pregnenediones/*pharmacology
Receptors
Steroid/*metabolism
Subfamily B
Transcription Factors/*antagonists & inhibitors/metabolism
Transcriptional Activation/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
6841–6851
Issue
8
Volume
73
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Neural stem cells as engraftable packaging lines can mediate gene delivery to microglia: evidence from studying retroviral env-related neurodegeneration.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-08
Subject
The topic of the resource
Animals; Mice; Cell Line; *Gene Transfer Techniques; Retroviridae Infections/pathology/*virology; *Microglia/cytology; *Stem Cells/cytology; Hematopoietic Stem Cell Transplantation; Nerve Degeneration; Retroviridae/genetics/*physiology; *Genes; env
Creator
An entity primarily responsible for making the resource
Lynch W P; Sharpe A H; Snyder E Y
Description
An account of the resource
The induction of spongiform myeloencephalopathy by murine leukemia viruses is mediated primarily by infection of central nervous system (CNS) microglia. In this regard, we have previously shown that CasBrE-induced disease requires late, rather than early, virus replication events in microglial cells (W. P. Lynch et al., J. Virol. 70:8896-8907, 1996). Furthermore, neurodegeneration requires the presence of unique sequences within the viral env gene. Thus, the neurodegeneration-inducing events could result from microglial expression of retroviral envelope protein alone or from the interaction of envelope protein with other viral structural proteins in the virus assembly and maturation process. To distinguish between these possible mechanisms of disease induction, we engineered the engraftable neural stem cell line C17-2 into packaging/producer cells in order to deliver the neurovirulent CasBrE env gene to endogenous CNS cells. This strategy resulted in significant CasBrE env expression within CNS microglia without the appearance of replication competent virus. CasBrE envelope expression within microglia was accompanied by increased expression of activation markers F4/80 and Mac-1 (CD11b) but failed to induce spongiform neurodegenerative changes. These results suggest that envelope expression alone within microglia is not sufficient to induce neurodegeneration. Rather, microglia-mediated disease appears to require neurovirulent Env protein interaction with other viral proteins during assembly or maturation. More broadly, the results presented here prove the efficacy of a novel method by which neural stem cell biology may be harnessed for genetically manipulating the CNS, not only for studying neurodegeneration but also as a paradigm for the disseminated distribution of retroviral vector-transduced genes.
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Transfer Techniques
*Genes
*Microglia/cytology
*Stem Cells/cytology
1999
Animals
Cell Line
env
Hematopoietic Stem Cell Transplantation
Journal of virology
Lynch W P
Mice
Nerve Degeneration
Retroviridae Infections/pathology/*virology
Retroviridae/genetics/*physiology
Sharpe A H
Snyder E Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
71–82
Volume
313
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Regulation of human sterol 27-hydroxylase gene (CYP27A1) by bile acids and hepatocyte nuclear factor 4alpha (HNF4alpha).
Publisher
An entity responsible for making the resource available
Gene
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
2003-08
Subject
The topic of the resource
Humans; Cell Line; Transfection; Gene Expression Regulation/drug effects; Base Sequence; Binding Sites/genetics; Response Elements/genetics; Molecular Sequence Data; Mutation; Chenodeoxycholic Acid/pharmacology; Transcription Factors/genetics/*metabolism; Hepatocyte Nuclear Factor 4; Mutagenesis; *DNA-Binding Proteins; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Bile Acids and Salts/*pharmacology; Cholestanetriol 26-Monooxygenase; DNA/chemistry/genetics; Luciferases/genetics/metabolism; Phosphoproteins/genetics/*metabolism; Recombinant Fusion Proteins/genetics/metabolism; Steroid Hydroxylases/*genetics; DNA; Dose-Response Relationship; Drug; Cultured; Receptors; Tumor Cells; Cloning; Molecular; Sequence Analysis; Promoter Regions; Genetic/*genetics; Cytoplasmic and Nuclear/genetics/metabolism; Site-Directed
Creator
An entity primarily responsible for making the resource
Chen Wenling; Chiang John Y L
Description
An account of the resource
Mitochondrial sterol 27-hydroxylase (CYP27A1) catalyses sterol side-chain oxidation of bile acid synthesis from cholesterol, and the first reaction of the acidic bile acid biosynthetic pathway. Hydrophobic bile acids suppress human CYP27A1 gene reporter activity when assayed in human hepatocellular blastoma HepG2 cells. Bile acids also inhibit CYP27A1 reporter activity in human embryonic kidney 293 cells. A putative bile acid response element (BARE) was mapped to a region downstream of nt -147 of the human CYP27A1 gene, within which a binding site for a liver-specific nuclear receptor, HNF4alpha, is identified. HNF4alpha strongly stimulates CYP27A1 gene transcription and mutation of its binding site markedly reduced promoter activity. Results suggest that human CYP27A1 gene transcription is suppressed by bile acids and HNF4alpha plays a pivotal role in transcriptional regulation of this gene.
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*DNA-Binding Proteins
2003
Base Sequence
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Bile Acids and Salts/*pharmacology
Binding Sites/genetics
Cell Line
Chen Wenling
Chenodeoxycholic Acid/pharmacology
Chiang John Y L
Cholestanetriol 26-Monooxygenase
Cloning
Cultured
Cytoplasmic and Nuclear/genetics/metabolism
Department of Integrative Medical Sciences
DNA
DNA/chemistry/genetics
Dose-Response Relationship
Drug
gene
Gene Expression Regulation/drug effects
Genetic/*genetics
Hepatocyte Nuclear Factor 4
Humans
Luciferases/genetics/metabolism
Molecular
Molecular Sequence Data
Mutagenesis
Mutation
NEOMED College of Medicine
Phosphoproteins/genetics/*metabolism
Promoter Regions
Receptors
Recombinant Fusion Proteins/genetics/metabolism
Response Elements/genetics
Sequence Analysis
Site-Directed
Steroid Hydroxylases/*genetics
Transcription Factors/genetics/*metabolism
Transfection
Tumor Cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
1402–1412
Issue
9
Volume
42
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nuclear receptor-mediated repression of human cholesterol 7alpha-hydroxylase gene transcription by bile acids.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-09
Subject
The topic of the resource
Humans; Animals; Rats; Cell Line; Transfection; Liver/metabolism; Reverse Transcriptase Polymerase Chain Reaction; DNA/metabolism; CHO Cells; Cricetinae; Cholesterol 7-alpha-Hydroxylase/*genetics; Bile Acids and Salts/*pharmacology; *Membrane Glycoproteins; *Hydroxysteroid Dehydrogenases; Caco-2 Cells; Carrier Proteins/genetics/physiology; DNA-Binding Proteins/drug effects/genetics/physiology; Gene Expression/*drug effects; Kidney; Luciferases/genetics; Recombinant Fusion Proteins/metabolism; Retinoid X Receptors; Taurocholic Acid/pharmacology; Transcription Factors/drug effects/genetics/physiology; Cultured; Receptors; RNA; Genetic/drug effects; Messenger/analysis; Transcription; Genetic; Tumor Cells; Promoter Regions; Embryo; Cytoplasmic and Nuclear/genetics/*physiology; Mammalian; Retinoic Acid/genetics/physiology
Creator
An entity primarily responsible for making the resource
Chen W; Owsley E; Yang Y; Stroup D; Chiang J Y
Description
An account of the resource
Hydrophobic bile acids strongly repressed transcription of the human cholesterol 7alpha-hydroxylase gene (CYP7A1) in the bile acid biosynthetic pathway in the liver. Farnesoid X receptor (FXR) repressed CYP7A1/Luc reporter activity in a transfection assay in human liver-derived HepG2 cells, but not in human embryonic kidney (HEK) 293 cells. FXR-binding activity was required for bile acid repression of CYP7A1 transcription despite the fact that FXR did not bind to the CYP7A1 promoter. FXR-induced liver-specific factors must be required for mediating bile acid repression. Bile acids and FXR repressed endogenous CYP7A1 but stimulated alpha-fetoprotein transcription factor (FTF) and small heterodimer partner (SHP) mRNA expression in HepG2 cells. Feeding of rats with chenodeoxycholic acid repressed CYP7A1, induced FTF, but had no effect on SHP mRNA expression in the liver. FTF strongly repressed CYP7A1 transcription in a dose-dependent manner, and SHP further inhibited CYP7A1 in HepG2 cells, but not in HEK 293 cells. FXR only moderately stimulated SHP transcription, whereas FTF strongly inhibited SHP transcription in HepG2 cells. Results revealed that FTF was a dominant negative factor that was induced by bile acid-activated FXR to inhibit both CYP7A1 and SHP transcription. Differential regulation of FTF and SHP expression by bile acids may explain the wide variation in CYP7A1 expression and the rate of bile acid synthesis and regulation in different species.
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Hydroxysteroid Dehydrogenases
*Membrane Glycoproteins
2001
Animals
Bile Acids and Salts/*pharmacology
Caco-2 Cells
Carrier Proteins/genetics/physiology
Cell Line
Chen W
Chiang J Y
CHO Cells
Cholesterol 7-alpha-Hydroxylase/*genetics
Cricetinae
Cultured
Cytoplasmic and Nuclear/genetics/*physiology
Department of Integrative Medical Sciences
DNA-Binding Proteins/drug effects/genetics/physiology
DNA/metabolism
Embryo
Gene Expression/*drug effects
Genetic
Genetic/drug effects
Humans
Journal of lipid research
Kidney
Liver/metabolism
Luciferases/genetics
Mammalian
Messenger/analysis
NEOMED College of Medicine
Owsley E
Promoter Regions
Rats
Receptors
Recombinant Fusion Proteins/metabolism
Retinoic Acid/genetics/physiology
Retinoid X Receptors
Reverse Transcriptase Polymerase Chain Reaction
RNA
Stroup D
Taurocholic Acid/pharmacology
Transcription
Transcription Factors/drug effects/genetics/physiology
Transfection
Tumor Cells
Yang Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3109/10837450.2015.1041043" target="_blank" rel="noreferrer noopener">http://doi.org/10.3109/10837450.2015.1041043</a>
Pages
647–654
Issue
6
Volume
21
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Gelucire-stabilized nanoparticles as a potential DNA delivery system.
Publisher
An entity responsible for making the resource available
Pharmaceutical development and technology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Humans; Animals; Mice; nanoparticles; Cell Line; Hep G2 Cells; gene therapy; *Gene Transfer Techniques; Cationic lipids; Cell Survival/drug effects/physiology; DNA/*administration & dosage/chemistry; macrophage activation; Macrophages/drug effects/physiology; Nanoparticles/*administration & dosage/chemistry; Polyethylene Glycols/*administration & dosage/chemistry; transfection
Creator
An entity primarily responsible for making the resource
Oyewumi Moses O; Wehrung Daniel; Sadana Prabodh
Description
An account of the resource
Clinical viability of gene delivery systems has been greatly impacted by potential toxicity of the delivery systems. Recently, we reported the nanoparticle (NP) preparation process that employs biocompatible materials such as Gelucire(R) 44/14 and cetyl alcohol as matrix materials. In the current study, the NP preparation was modified for pDNA loading through: (i) inclusion of cationic lipids (DOTAP or DDAB) with NP matrix materials; or (ii) application of cationic surfactants (CTAB) to generate NPs with desired surface charges for pDNA complexation. Colloidal stability and efficiency of loading pGL3-DR4X2-luciferase plasmid DNA in NPs were verified by gel permeation chromatography. Compared to pDNA alone, all the NPs were effective in preserving pDNA from digestion by DNase. While pDNA loading using CTAB-NPs involved fewer steps compared to
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3109/10837450.2015.1041043" target="_blank" rel="noreferrer noopener">10.3109/10837450.2015.1041043</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Transfer Techniques
2016
Animals
Cationic lipids
Cell Line
Cell Survival/drug effects/physiology
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
DNA/*administration & dosage/chemistry
gene therapy
Hep G2 Cells
Humans
macrophage activation
Macrophages/drug effects/physiology
Mice
Nanoparticles
Nanoparticles/*administration & dosage/chemistry
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Oyewumi Moses O
Pharmaceutical development and technology
Polyethylene Glycols/*administration & dosage/chemistry
Sadana Prabodh
Transfection
Wehrung Daniel
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3109/10837450.2014.892130" target="_blank" rel="noreferrer noopener">http://doi.org/10.3109/10837450.2014.892130</a>
Pages
497–506
Issue
4
Volume
20
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Brain-targeted delivery of doxorubicin using glutathione-coated nanoparticles for brain cancers.
Publisher
An entity responsible for making the resource available
Pharmaceutical development and technology
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-06
Subject
The topic of the resource
Antibiotics; Animals; *Drug Delivery Systems; Rats; Cell Line; Polylactic Acid-Polyglycolic Acid Copolymer; Blood-Brain Barrier/*metabolism; Brain cancer; Brain Neoplasms/drug therapy/metabolism; brain-targeted delivery; doxorubicin; Doxorubicin/*administration & dosage/pharmacokinetics; Drug Carriers/*chemistry/metabolism; Glutathione/*chemistry/metabolism; Lactic Acid/chemistry/metabolism; Nanoparticles/*chemistry/metabolism; PLGA-PEG NP; Polyethylene Glycols/chemistry/metabolism; Polyglycolic Acid/chemistry/metabolism; Tumor; Antineoplastic/*administration & dosage/pharmacokinetics
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner; Wehrung Daniel; Groshev Anastasia; Hirani Anjali; Sutariya Vijaykumar
Description
An account of the resource
OBJECTIVES: To prepare and characterize in vitro a novel brain-targeted delivery of doxorubicin using glutathione-coated nanoparticles (NPs) for the treatment of brain cancer. METHODS: Doxorubicin-loaded NPs were prepared by the nanoprecipitation method using PLGA-COOH (dl-lactide-co-glycolide). The NPs were coated with a glutathione-PEG conjugate (PEG-GSH) in order to target delivery to the brain. The NPs were characterized via in vitro studies to determine particle size, drug release, cellular uptake, immunofluorescence study, cytotoxic assay, and in vitro blood-brain barrier (BBB) assay. RESULTS: The NPs showed a particle size suitable for BBB permeation (particle size around 200 nm). The in vitro release profile of the NPs exhibited no initial burst release and showed sustained drug release for up to 96 h. The immunofluorescence study showed the glutathione coating does not interfere with the drug release. Furthermore, in vitro BBB Transwell study showed significantly higher permeation of the doxorubicin-loaded NPs compared with the free doxorubicin solution through the coculture of rat brain endothelial (RBE4) and C6 astrocytoma cells (p \textless 0.05). CONCLUSIONS: We conclude that the initial in vitro characterization of the NPs demonstrates potential in delivering doxorubicin to cancer cells with possible future application in targeting brain cancers in vivo.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3109/10837450.2014.892130" target="_blank" rel="noreferrer noopener">10.3109/10837450.2014.892130</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Drug Delivery Systems
2015
Animals
Antibiotics
Antineoplastic/*administration & dosage/pharmacokinetics
Blood-Brain Barrier/*metabolism
Brain cancer
Brain Neoplasms/drug therapy/metabolism
brain-targeted delivery
Cell Line
Doxorubicin
Doxorubicin/*administration & dosage/pharmacokinetics
Drug Carriers/*chemistry/metabolism
Geldenhuys Werner
Glutathione/*chemistry/metabolism
Groshev Anastasia
Hirani Anjali
Lactic Acid/chemistry/metabolism
Nanoparticles/*chemistry/metabolism
Pharmaceutical development and technology
PLGA-PEG NP
Polyethylene Glycols/chemistry/metabolism
Polyglycolic Acid/chemistry/metabolism
Polylactic Acid-Polyglycolic Acid Copolymer
Rats
Sutariya Vijaykumar
Tumor
Wehrung Daniel
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3109/1061186X.2011.589435" target="_blank" rel="noreferrer noopener">http://doi.org/10.3109/1061186X.2011.589435</a>
Pages
837–845
Issue
9
Volume
19
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Brain-targeted delivery of paclitaxel using glutathione-coated nanoparticles for brain cancers.
Publisher
An entity responsible for making the resource available
Journal of drug targeting
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-11
Subject
The topic of the resource
Humans; Male; Animals; Mice; *Drug Delivery Systems; Rats; Cell Line; Nanoparticles; Permeability; Particle Size; Delayed-Action Preparations; Blood-Brain Barrier/metabolism; Adenosine Triphosphatases/metabolism; Brain Neoplasms/drug therapy; Cell Death/drug effects; Coumarins/administration & dosage/pharmacokinetics; Glioma/drug therapy/pathology; Glutathione/*chemistry; Microtubules/metabolism; Paclitaxel/administration & dosage/*pharmacokinetics/pharmacology; Thiazoles/administration & dosage/pharmacokinetics; Tubulin/metabolism; Inbred C57BL; Tumor; ATP Binding Cassette Transporter; Antineoplastic Agents; Member 1/metabolism; Subfamily B; Phytogenic/administration & dosage/*pharmacokinetics/pharmacology
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner; Mbimba Thomas; Bui Thong; Harrison Kimberly; Sutariya Vijaykumar
Description
An account of the resource
Paclitaxel is not effective for treatment of brain cancers because it cannot cross the blood-brain barrier (BBB) due to efflux by P-glycoprotein (P-gp). In this work, glutathione-coated poly-(lactide-co-glycolide) (PLGA) nanoparticles (NPs) of paclitaxel were developed for brain targeting for treatment of brain cancers. P-gp ATPase assay was used to evaluate the NP as potential substrates. The NP showed a particle size suitable for BBB permeation (particle size around 200 nm) and higher cellular uptake of the NP was demonstrated in RG2 cells. The
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3109/1061186X.2011.589435" target="_blank" rel="noreferrer noopener">10.3109/1061186X.2011.589435</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Drug Delivery Systems
2011
Adenosine Triphosphatases/metabolism
Animals
Antineoplastic Agents
ATP Binding Cassette Transporter
Blood-Brain Barrier/metabolism
Brain Neoplasms/drug therapy
Bui Thong
Cell Death/drug effects
Cell Line
Coumarins/administration & dosage/pharmacokinetics
Delayed-Action Preparations
Geldenhuys Werner
Glioma/drug therapy/pathology
Glutathione/*chemistry
Harrison Kimberly
Humans
Inbred C57BL
Journal of drug targeting
Male
Mbimba Thomas
Member 1/metabolism
Mice
Microtubules/metabolism
Nanoparticles
Paclitaxel/administration & dosage/*pharmacokinetics/pharmacology
Particle Size
Permeability
Phytogenic/administration & dosage/*pharmacokinetics/pharmacology
Rats
Subfamily B
Sutariya Vijaykumar
Thiazoles/administration & dosage/pharmacokinetics
Tubulin/metabolism
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3109/10611861003639796" target="_blank" rel="noreferrer noopener">http://doi.org/10.3109/10611861003639796</a>
Pages
665–674
Issue
9
Volume
18
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Brain-targeted delivery of Tempol-loaded nanoparticles for neurological disorders.
Publisher
An entity responsible for making the resource available
Journal of drug targeting
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-11
Subject
The topic of the resource
Animals; Rats; Cell Line; Nanoparticles; Polylactic Acid-Polyglycolic Acid Copolymer; Particle Size; Delayed-Action Preparations; Antibodies; Polyethylene Glycols; Blood-Brain Barrier/metabolism; *Lactic Acid; *Polyglycolic Acid; Antioxidants/chemistry/*metabolism; Cross-Linking Reagents/chemistry; Cyclic N-Oxides/chemistry/*metabolism; Free Radical Scavengers/chemistry/*metabolism; Maleimides/chemistry; Spin Labels; Transferrin/*immunology; Tumor; Monoclonal/chemistry/*metabolism
Creator
An entity primarily responsible for making the resource
Carroll Richard T; Bhatia Deepak; Geldenhuys Werner; Bhatia Ruchi; Miladore Nicholas; Bishayee Anupam; Sutariya Vijaykumar
Description
An account of the resource
Brain-targeted Tempol-loaded poly-(lactide-co-glycolide) (PLGA) nanoparticles (NPs) conjugated with a transferrin antibody (OX 26) were developed using the nanoprecipitation method. These NPs may have utility in treating neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Central to these diseases is an increased production of reactive oxygen and nitrogen species which may take part in the development of these conditions. As proof of principle, the NPs were loaded with Tempol, a free radical scavenger that has been shown to be protective against oxidative insults. To enhance the delivery of NPs to the central nervous system (CNS), we conjugated the transferrin receptor antibody covalently to PLGA NPs using the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3109/10611861003639796" target="_blank" rel="noreferrer noopener">10.3109/10611861003639796</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lactic Acid
*Polyglycolic Acid
2010
Animals
Antibodies
Antioxidants/chemistry/*metabolism
Bhatia Deepak
Bhatia Ruchi
Bishayee Anupam
Blood-Brain Barrier/metabolism
Carroll Richard T
Cell Line
Cross-Linking Reagents/chemistry
Cyclic N-Oxides/chemistry/*metabolism
Delayed-Action Preparations
Free Radical Scavengers/chemistry/*metabolism
Geldenhuys Werner
Journal of drug targeting
Maleimides/chemistry
Miladore Nicholas
Monoclonal/chemistry/*metabolism
Nanoparticles
Particle Size
Polyethylene Glycols
Polylactic Acid-Polyglycolic Acid Copolymer
Rats
Spin Labels
Sutariya Vijaykumar
Transferrin/*immunology
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.2174/1568009617666161121123948" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1568009617666161121123948</a>
Pages
479–485
Issue
5
Volume
17
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Identification of Novel Agents for the Treatment of Brain Metastases of Breast Cancer.
Publisher
An entity responsible for making the resource available
Current cancer drug targets
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-7
Subject
The topic of the resource
Female; Humans; Animals; Mice; Apoptosis; Cell Line; ADME; Antineoplastic Agents/*therapeutic use; brain cancer; Brain Neoplasms/*drug therapy/pathology/*secondary; Breast Neoplasms/*pathology; chemotherapy; CNS; distribution; drug discovery; Drug resistance; Tumor
Creator
An entity primarily responsible for making the resource
Venishetty Vinay K; Geldenhuys Werner J; Terell-Hall Tori B; Griffith Jessica I G; Sondag Gregory R; Safadi Fayez F; Lockman Paul R
Description
An account of the resource
BACKGROUND: Brain cancer from metastasized breast cancer has a high mortality rate in women. The treatment of lesions is hampered in large part by the blood-brain barrier (BBB), which prevents adequate distribution of anti-cancer compounds to brain metastases. METHOD: In this study we used a novel screening method to identify candidate molecules that are well-suited to utilizing the BBB choline transporter for distribution into the brain parenchyma. RESULTS: From our screen we identified two compounds, Ch-1 and Ch-2 that were able to reduce the brain tumor burden in a murine mouse model of brain metastasis of breast cancer. These compounds also significantly increased the survival of mice by more than 10 days. Mechanistic studies indicated that Ch-1 is able to prevent the activation of the pro-survival mitogen-activated kinases (MAPKs) by osteoactivin (OA; Glycoprotein nonmetastatic melanoma protein B GPNMB). CONCLUSION: The results from this study show that nutrient transporter virtual screening is a viable novel alternative to traditional drug screening programs to identify anti-cancer compounds for the treatment of brain cancers.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/1568009617666161121123948" target="_blank" rel="noreferrer noopener">10.2174/1568009617666161121123948</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
ADME
Animals
Antineoplastic Agents/*therapeutic use
Apoptosis
Brain cancer
Brain Neoplasms/*drug therapy/pathology/*secondary
Breast Neoplasms/*pathology
Cell Line
Chemotherapy
CNS
Current cancer drug targets
Department of Anatomy & Neurobiology
distribution
Drug Discovery
Drug Resistance
Female
Geldenhuys Werner J
Griffith Jessica I G
Humans
Lockman Paul R
Mice
NEOMED College of Medicine
Safadi Fayez F
Sondag Gregory R
Terell-Hall Tori B
Tumor
Venishetty Vinay K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.2676" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.2676</a>
Pages
1286–1301
Issue
2
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A class of genes in the HER2 regulon that is poised for transcription in breast cancer cell lines and expressed in human breast tumors.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-01
Subject
The topic of the resource
Humans; Cell Line; *Gene Expression Regulation; Reverse Transcriptase Polymerase Chain Reaction; *Gene Expression Profiling; Breast Neoplasms/genetics/pathology; Gene Regulatory Networks; Homeodomain Proteins/genetics/metabolism; MCF-7 Cells; Nanog Homeobox Protein; Neoplastic Stem Cells/metabolism; Octamer Transcription Factor-3/genetics/metabolism; Regulon/*genetics; RNA Polymerase II/metabolism; SOXB1 Transcription Factors/genetics/metabolism; Tumor Microenvironment/genetics; Receptor; Blotting; Western; Tumor; Neoplastic; ErbB-2/*genetics/metabolism
Creator
An entity primarily responsible for making the resource
Rahmatpanah Farah B; Jia Zhenyu; Chen Xin; Char Jessica E; Men Bozhao; Franke Anna-Clara; Jones Frank E; McClelland Michael; Mercola Dan
Description
An account of the resource
HER2-positive breast cancer accounts for 25% of all cases and has a poor prognosis. Although progress has been made in understanding signal transduction, little is known of how HER2 achieves gene regulation. We performed whole genome expression analysis on a HER2(+) and HER2(-) breast cancer cell lines and compared these results to expression in 812 primary tumors stratified by their HER2 expression level. Chip-on-chip with anti-RNA polymerase II was compared among breast cancer cell lines to identify genes that are potentially activated by HER2. The expression levels of these HER2-dependent POL II binding genes were determined for the 812 HER2+/- breast cancer tissues. Genes differentially expressed between HER2+/- cell lines were generally regulated in the same direction as in breast cancer tissues. We identified genes that had POLII binding in HER2(+) cell lines, but without significant gene expression. Of 737 such genes "poised" for expression in cell lines, 113 genes were significantly differentially expressed in breast tumors in a HER2-dependent manner. Pathway analysis of these 113 genes revealed that a large group of genes were associated with stem cell and progenitor cell control as indicated by networks centered on NANOG, SOX2, OCT3/4. HER2 directs POL II binding to a large number of genes in breast cancer cells. A "poised" class of genes in HER2(+) cell lines with POLII binding and low RNA expression but is differentially expressed in primary tumors, strongly suggests a role of the microenvironment and further suggests a role for stem cells proliferation in HER2-regulated breast cancer tissue.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.2676" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.2676</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Profiling
*Gene Expression Regulation
2015
Blotting
Breast Neoplasms/genetics/pathology
Cell Line
Char Jessica E
Chen Xin
ErbB-2/*genetics/metabolism
Franke Anna-Clara
Gene Regulatory Networks
Homeodomain Proteins/genetics/metabolism
Humans
Jia Zhenyu
Jones Frank E
McClelland Michael
MCF-7 Cells
Men Bozhao
Mercola Dan
Nanog Homeobox Protein
Neoplastic
Neoplastic Stem Cells/metabolism
Octamer Transcription Factor-3/genetics/metabolism
Oncotarget
Rahmatpanah Farah B
Receptor
Regulon/*genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA Polymerase II/metabolism
SOXB1 Transcription Factors/genetics/metabolism
Tumor
Tumor Microenvironment/genetics
Western
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.1995" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.1995</a>
Pages
3862–3870
Issue
11
Volume
5
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Sequential activation of Elk-1/Egr-1/GADD45alpha by arsenic.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-06
Subject
The topic of the resource
Humans; Cell Line; Proto-Oncogene Proteins c-akt/metabolism; MAP Kinase Signaling System; Arsenic/*pharmacology; Bronchi/cytology/drug effects/metabolism; Cell Cycle Proteins/biosynthesis/genetics/*metabolism; Early Growth Response Protein 1/biosynthesis/genetics/*metabolism; Epithelial Cells/drug effects/metabolism; ets-Domain Protein Elk-1/biosynthesis/genetics/*metabolism; Nuclear Proteins/biosynthesis/genetics/*metabolism; RNA; Genetic; Promoter Regions; Messenger/biosynthesis/genetics
Creator
An entity primarily responsible for making the resource
Shi Qiwen; Sutariya Vijaykumar; Bishayee Anupam; Bhatia Deepak
Description
An account of the resource
Long-term exposure to arsenic, an environmental contaminant, leads to increased risks of cancers. In the present study, we investigated the sequential regulation of Elk-1 and Egr-1 on As3+-induced GADD45alpha, an effector of G2/M checkpoint. We found that As3+ transcriptionally induced both Elk-1 and Egr-1, and NF-kappaB binding site was necessary for As3+-induced Egr-1 promoter activity. However, specific inhibition of JNK, ERK, and Elk-1 inhibited Egr-1 induction. Furthermore, silencing of Egr-1 downregulated As3+-induced expression of GADD45alpha and ChIP assay confirmed the direct binding of Egr-1 to GADD45alpha promoter. Taken together, our data indicated that the increase of GADD45alpha in response to As3+ was mediated sequentially by Elk-1 and Egr-1.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.1995" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.1995</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Arsenic/*pharmacology
Bhatia Deepak
Bishayee Anupam
Bronchi/cytology/drug effects/metabolism
Cell Cycle Proteins/biosynthesis/genetics/*metabolism
Cell Line
Early Growth Response Protein 1/biosynthesis/genetics/*metabolism
Epithelial Cells/drug effects/metabolism
ets-Domain Protein Elk-1/biosynthesis/genetics/*metabolism
Genetic
Humans
MAP Kinase Signaling System
Messenger/biosynthesis/genetics
Nuclear Proteins/biosynthesis/genetics/*metabolism
Oncotarget
Promoter Regions
Proto-Oncogene Proteins c-akt/metabolism
RNA
Shi Qiwen
Sutariya Vijaykumar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0166560</a>
Pages
e0166560–e0166560
Issue
11
Volume
11
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Salvianolic Acid B Alleviates Heart Failure by Inactivating ERK1/2/GATA4 Signaling Pathway after Pressure Overload in Mice.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016
Subject
The topic of the resource
Male; Animals; Mice; Phosphorylation/drug effects; Signal Transduction/*drug effects; Rats; Cell Line; Proto-Oncogene Proteins c-akt/metabolism; Benzofurans/chemistry/*pharmacology; Blood Pressure/drug effects; GATA4 Transcription Factor/metabolism; Heart Failure/metabolism/*pathology; Heart Ventricles/diagnostic imaging; Mitogen-Activated Protein Kinase 1/metabolism; Mitogen-Activated Protein Kinase 3/metabolism; Myocardium/metabolism/pathology; Drugs; Inbred C57BL; Animal; Disease Models; Myocytes; Aorta; Brain/blood; Natriuretic Peptide; Cardiac/cytology/drug effects/metabolism; Chinese Herbal/chemistry/pharmacology; Thoracic/surgery
Creator
An entity primarily responsible for making the resource
Yu Juan; Chen Renshan; Tan Yafang; Wu Jiashin; Qi Jianyong; Zhang Minzhou; Gu Weiwang
Description
An account of the resource
BACKGROUND: Heart failure(HF) is a dangerous disease that affects millions of patients. Radix Salvia is widely used in Chinese clinics to treat heart diseases. Salvianolic acid B(SalB) is the major active component of Radix Salvia. This study investigated the mechanisms of action and effects of SalB on HF in an experimental mouse model of HF. METHODS: We created a mouse model of HF by inducing pressure overload with transverse aortic constriction(TAC) surgery for 2 weeks and compared among 4 study groups: SHAM group (n = 10), TAC group (n = 9), TAC+MET group (metprolol, positive drug treatment, n = 9) and TAC+SalB group (SalB, 240 mg*kg-1*day-1, n = 9). Echocardiography was used to evaluate the dynamic changes in cardiac structure and function in vivo. Plasma brain natriuretic peptide (BNP) concentration was detected by Elisa method. In addition, H9C2 rat cardiomyocytes were cultured and Western blot were implemented to evaluate the phosphorylation of ERK1/2, AKT, and protein expression of GATA4. RESULTS: SalB significantly inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, but not Ser473 site of AKT, subsequently inhibited protein expression of GATA4 and plasma BNP(P \textless 0.001), and then inhibited HF at 2 weeks after TAC surgery. CONCLUSIONS: Our data provide a mechanism of inactivating the ERK1/2/GATA4 signaling pathway for SalB inhibition of the TAC-induced HF.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0166560</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Animal
Animals
Aorta
Benzofurans/chemistry/*pharmacology
Blood Pressure/drug effects
Brain/blood
Cardiac/cytology/drug effects/metabolism
Cell Line
Chen Renshan
Chinese Herbal/chemistry/pharmacology
Disease Models
Drugs
GATA4 Transcription Factor/metabolism
Gu Weiwang
Heart Failure/metabolism/*pathology
Heart Ventricles/diagnostic imaging
Inbred C57BL
Male
Mice
Mitogen-Activated Protein Kinase 1/metabolism
Mitogen-Activated Protein Kinase 3/metabolism
Myocardium/metabolism/pathology
Myocytes
Natriuretic Peptide
Phosphorylation/drug effects
PloS one
Proto-Oncogene Proteins c-akt/metabolism
Qi Jianyong
Rats
Signal Transduction/*drug effects
Tan Yafang
Thoracic/surgery
Wu Jiashin
Yu Juan
Zhang Minzhou
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0115919" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0115919</a>
Pages
e0115919–e0115919
Issue
1
Volume
10
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MiR-21 enhances melanoma invasiveness via inhibition of tissue inhibitor of metalloproteinases 3 expression: in vivo effects of MiR-21 inhibitor.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Humans; Gene Expression Regulation; Cell Line; MicroRNAs/*genetics/metabolism; Cell Movement/genetics; Cell Proliferation/genetics; Melanoma/*genetics/metabolism/pathology; Neoplasm Invasiveness/*genetics/pathology; Skin Neoplasms/*genetics/metabolism/pathology; Tissue Inhibitor of Metalloproteinase-3/*genetics/metabolism; RNA; Tumor; Neoplastic; Small Interfering
Creator
An entity primarily responsible for making the resource
Martin del Campo Sara E; Latchana Nicholas; Levine Kala M; Grignol Valerie P; Fairchild Ene T; Jaime-Ramirez Alena Cristina; Dao Thao-Vi; Karpa Volodymyr I; Carson Mary; Ganju Akaansha; Chan Anthony N; Carson William E 3rd
Description
An account of the resource
Metastatic melanoma is the most aggressive form of this cancer. It is important to understand factors that increase or decrease metastatic activity in order to more effectively research and implement treatments for melanoma. Increased cell invasion through the extracellular matrix is required for metastasis and is enhanced by matrix metalloproteinases (MMPs). Tissue inhibitor of metalloproteinases 3 (TIMP3) inhibits MMP activity. It was previously shown by our group that miR-21, a potential regulator of TIMP3, is over-expressed in cutaneous melanoma. It was therefore hypothesized that increased levels of miR-21 expression would lead to decreased expression of TIMP3 and thereby enhance the invasiveness of melanoma cells. miR-21 over-expression in the melanoma cell lines WM1552c, WM793b, A375 and MEL 39 was accomplished via transfection with pre-miR-21. Immunoblot analysis of miR-21-overexpressing cell lines revealed reduced expression of TIMP3 as compared to controls. This in turn led to a significant increase in the invasiveness of the radial growth phase cell line WM1552c and the vertical growth phase cell line WM793b (p \textless 0.05), but not in the metastatic cell lines A375 or MEL 39. The proliferation and migration of miR-21 over-expressing cell lines was not affected. Reduced expression of TIMP3 was achieved by siRNA knockdown and significantly enhanced invasion of melanoma cell lines, mimicking the effects of miR-21 over-expression. Treatment of tumor cells with a linked nucleic acid antagomir to miR-21 inhibited tumor growth and increased tumor expression of TIMP3 in vivo in 01B74 Athymic NCr-nu/nu mice. Intra-tumoral injections of anti-miR-21 produced similar effects. This data shows that increased expression of miR-21 enhanced the invasive potential of melanoma cell lines through TIMP3 inhibition. Therefore, inhibition of miR-21 in melanoma may reduce melanoma invasiveness.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0115919" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0115919</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Carson Mary
Carson William E 3rd
Cell Line
Cell Movement/genetics
Cell Proliferation/genetics
Chan Anthony N
Dao Thao-Vi
Fairchild Ene T
Ganju Akaansha
Gene Expression Regulation
Grignol Valerie P
Humans
Jaime-Ramirez Alena Cristina
Karpa Volodymyr I
Latchana Nicholas
Levine Kala M
Martin del Campo Sara E
Melanoma/*genetics/metabolism/pathology
MicroRNAs/*genetics/metabolism
Neoplasm Invasiveness/*genetics/pathology
Neoplastic
PloS one
RNA
Skin Neoplasms/*genetics/metabolism/pathology
Small Interfering
Tissue Inhibitor of Metalloproteinase-3/*genetics/metabolism
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0115325" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0115325</a>
Pages
e0115325–e0115325
Issue
2
Volume
10
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Integrin mediated adhesion of osteoblasts to connective tissue growth factor (CTGF/CCN2) induces cytoskeleton reorganization and cell differentiation.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Animals; Mice; Signal Transduction; Cell Line; Cell Adhesion; *Cell Differentiation; Connective Tissue Growth Factor/chemistry/*metabolism; Core Binding Factor Alpha 1 Subunit/metabolism; Cytoskeleton/*metabolism; Extracellular Signal-Regulated MAP Kinases/metabolism; Focal Adhesion Protein-Tyrosine Kinases/metabolism; Integrins/*metabolism; Osteoblasts/*cytology/*metabolism; rac GTP-Binding Proteins/metabolism; Transcriptional Activation; Receptors; Vitronectin/metabolism
Creator
An entity primarily responsible for making the resource
Hendesi Honey; Barbe Mary F; Safadi Fayez F; Monroy M Alexandra; Popoff Steven N
Description
An account of the resource
Pre-osteoblast adhesion and interaction with extracellular matrix (ECM) proteins through integrin receptors result in activation of signaling pathways regulating osteoblast differentiation. Connective tissue growth factor (CTGF/CCN2) is a matricellular protein secreted into the ECM. Prior studies in various cell types have shown that cell adhesion to CTGF via integrin receptors results in activation of specific signaling pathways that regulate cell functions, such as differentiation and cytoskeletal reorganization. To date, there are no studies that have examined whether CTGF can serve as an adhesive substrate for osteoblasts. In this study, we used the MC3T3-E1 cell line to demonstrate that CTGF serves as an adhesive matrix for osteoblasts. Anti-integrin blocking experiments and co-immunoprecipitation assays demonstrated that the integrin alphavbeta1 plays a key role in osteoblast adhesion to a CTGF matrix. Immunofluorescence staining of osteoblasts cultured on a CTGF matrix confirmed actin cytoskeletal reorganization, enhanced spreading, formation of focal adhesions, and activation of Rac1. Alkaline phosphatase (ALP) staining and activity assays, as well as Alizarin red staining demonstrated that osteoblast attachment to CTGF matrix enhanced maturation, bone nodule formation and matrix mineralization. To investigate whether the effect of CTGF on osteoblast differentiation involves integrin-mediated activation of specific signaling pathways, we performed Western blot, chromatin immunoprecipitation (ChIP) and qPCR assays. Osteoblasts cultured on a CTGF matrix showed increased total and phosphorylated (activated) forms of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK). Inhibition of ERK blocked osteogenic differentiation in cells cultured on a CTGF matrix. There was an increase in runt-related transcription factor 2 (Runx2) binding to the osteocalcin gene promoter, and in the expression of osteogenic markers regulated by Runx2. Collectively, the results of this study are the first to demonstrate CTGF serves as a suitable matrix protein, enhancing osteoblast adhesion (via alphavbeta1 integrin) and promoting cell spreading via cytoskeletal reorganization and Rac1 activation. Furthermore, integrin-mediated activation of ERK signaling resulted in increased osteoblast differentiation accompanied by an increase in Runx2 binding to the osteocalcin promoter and in the expression of osteogenic markers.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0115325" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0115325</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cell Differentiation
2015
Animals
Barbe Mary F
Cell Adhesion
Cell Line
Connective Tissue Growth Factor/chemistry/*metabolism
Core Binding Factor Alpha 1 Subunit/metabolism
Cytoskeleton/*metabolism
Department of Anatomy & Neurobiology
Extracellular Signal-Regulated MAP Kinases/metabolism
Focal Adhesion Protein-Tyrosine Kinases/metabolism
Hendesi Honey
Integrins/*metabolism
Mice
Monroy M Alexandra
NEOMED College of Medicine
Osteoblasts/*cytology/*metabolism
PloS one
Popoff Steven N
rac GTP-Binding Proteins/metabolism
Receptors
Safadi Fayez F
Signal Transduction
Transcriptional Activation
Vitronectin/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M800140-JLR200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M800140-JLR200</a>
Pages
1981–1989
Issue
9
Volume
49
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-09
Subject
The topic of the resource
*Gene Expression Regulation; Animals; Cell Line; Cholesterol 7-alpha-Hydroxylase/*genetics; Enzymologic; Forkhead Transcription Factors/physiology; Humans; Insulin/*physiology; Male; Nerve Tissue Proteins/physiology; Rats; Signal Transduction; Smad3 Protein/antagonists & inhibitors/pharmacology; Sprague-Dawley; Transforming Growth Factor beta1/*physiology; Tumor; Tumor Necrosis Factor-alpha/*physiology
Creator
An entity primarily responsible for making the resource
Li Tiangang; Ma Huiyan; Chiang John Y L
Description
An account of the resource
The TGFbeta1/Smad pathway plays a critical role in cholestasis and liver fibrosis. Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. In contrast to inhibition of human CYP7A1 gene transcription, TGFbeta1 stimulates rat Cyp7a1 reporter activity. Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. These results suggest a mechanistic basis for induction of Cyp7a1 activity and bile acid synthesis in cholestatic rats and in diabetic rats. The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M800140-JLR200" target="_blank" rel="noreferrer noopener">10.1194/jlr.M800140-JLR200</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2008
Animals
Cell Line
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics
Department of Integrative Medical Sciences
Enzymologic
Forkhead Transcription Factors/physiology
Humans
Insulin/*physiology
Journal of lipid research
Li Tiangang
Ma Huiyan
Male
NEOMED College of Medicine
Nerve Tissue Proteins/physiology
Rats
Signal Transduction
Smad3 Protein/antagonists & inhibitors/pharmacology
Sprague-Dawley
Transforming Growth Factor beta1/*physiology
Tumor
Tumor Necrosis Factor-alpha/*physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M600282-JLR200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M600282-JLR200</a>
Pages
373–384
Issue
2
Volume
48
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
PXR induces CYP27A1 and regulates cholesterol metabolism in the intestine.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-02
Subject
The topic of the resource
*Lipid Metabolism; ATP Binding Cassette Transporter; ATP Binding Cassette Transporter 1; ATP-Binding Cassette Transporters/genetics; Base Sequence; Cell Line; Cholestanetriol 26-Monooxygenase/*metabolism; Cholesterol; Cholesterol/*metabolism; Fluorinated; Genes; Genetic/drug effects; Genetic/genetics; HDL/metabolism; Hepatocytes/drug effects/enzymology/metabolism; Humans; Hydrocarbons; Hydroxycholesterols/metabolism/pharmacology; Intestinal Mucosa/metabolism; Intestines/cytology/drug effects/enzymology; Member 1; Messenger/genetics/metabolism; Molecular Sequence Data; Pregnane X Receptor; Promoter Regions; Receptors; Reporter; Response Elements/genetics; Rifampin/pharmacology; RNA; Steroid/*metabolism; Subfamily G; Sulfonamides/pharmacology; Transcription; Up-Regulation/drug effects
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chen Wenling; Chiang John Y L
Description
An account of the resource
Mitochondrial sterol 27-hydroxylase (CYP27A1) catalyzes oxidative cleavage of the sterol side chain in the bile acid biosynthetic pathway in the liver and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M600282-JLR200" target="_blank" rel="noreferrer noopener">10.1194/jlr.M600282-JLR200</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lipid Metabolism
2007
ATP Binding Cassette Transporter
ATP Binding Cassette Transporter 1
ATP-Binding Cassette Transporters/genetics
Base Sequence
Cell Line
Chen Wenling
Chiang John Y L
Cholestanetriol 26-Monooxygenase/*metabolism
Cholesterol
Cholesterol/*metabolism
Department of Integrative Medical Sciences
Fluorinated
Genes
Genetic/drug effects
Genetic/genetics
HDL/metabolism
Hepatocytes/drug effects/enzymology/metabolism
Humans
Hydrocarbons
Hydroxycholesterols/metabolism/pharmacology
Intestinal Mucosa/metabolism
Intestines/cytology/drug effects/enzymology
Journal of lipid research
Li Tiangang
Member 1
Messenger/genetics/metabolism
Molecular Sequence Data
NEOMED College of Medicine
Pregnane X Receptor
Promoter Regions
Receptors
Reporter
Response Elements/genetics
Rifampin/pharmacology
RNA
Steroid/*metabolism
Subfamily G
Sulfonamides/pharmacology
Transcription
Up-Regulation/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1186/1742-4690-7-93" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/1742-4690-7-93</a>
Pages
93–93
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Misfolding of CasBrE SU is reversed by interactions with 4070A Env: implications for gammaretroviral neuropathogenesis.
Publisher
An entity responsible for making the resource available
Retrovirology
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-11
Subject
The topic of the resource
Animals; Cell Line; env/*metabolism; Experimental/*virology; Gene Products; Helper Viruses/metabolism/pathogenicity/*physiology; Leukemia; Leukemia Virus; Mice; Motor Neuron Disease/*virology; Murine/metabolism/pathogenicity/*physiology; Neural Stem Cells/*virology; Protein Binding; Protein Folding; Protein Subunits/metabolism; Retroviridae Infections/*virology; Tumor Virus Infections/*virology; Virulence
Creator
An entity primarily responsible for making the resource
Li Ying; Lynch William P
Description
An account of the resource
BACKGROUND: CasBrE is a neurovirulent murine leukemia virus (MLV) capable of inducing paralytic disease with associated spongiform neurodegeneration. The neurovirulence of this virus has been genetically mapped to the surface expressed subunit (SU) of the env gene. However, CasBrE SU synthesized in the absence of the transmembrane subunit (TM) does not retain ecotropic receptor binding activity, indicating that folding of the receptor binding domain (RBD) requires this domain. Using a neural stem cell (NSC) based viral trans complementation approach to examine whether misfolded CasBrE SU retained neurovirulence, we observed CasBrE SU interaction with the "non-neurovirulent" amphotropic helper virus, 4070A which restored functional activity of CasBrE SU. RESULTS: Herein, we show that infection of NSCs expressing CasBrE SU with 4070A (CasES+4070A-NSCs) resulted in the redistribution of CasBrE SU from a strictly secreted product to include retention on the plasma membrane. Cell surface cross-linking analysis suggested that CasBrE SU membrane localization was due to interactions with 4070A Env. Viral particles produced from CasES+4070A-NSCS contained both CasBrE and 4070A gp70 Env proteins. These particles displayed ecotropic receptor-mediated infection, but were still 100-fold less efficient than CasE+4070A-NSC virus. Infectious center analysis showed CasBrE SU ecotropic transduction efficiencies approaching those of NSCs expressing full length CasBrE Env (CasE; SU+TM). In addition, CasBrE SU-4070A Env interactions resulted in robust ecotropic superinfection interference indicating near native intracellular SU interaction with its receptor, mCAT-1. CONCLUSIONS: In this report we provided evidence that 4070A Env and CasBrE SU physically interact within NSCs leading to CasBrE SU retention on the plasma membrane, incorporation into viral particles, restoration of mCAT-1 binding, and capacity for initiation of TM-mediated fusion events. Thus, heterotropic Env-SU interactions facilitates CasBrE SU folding events that restore Env activity. These findings are consistent with the idea that one protein conformation acts as a folding scaffold or nucleus for a second protein of similar primary structure, a process reminiscent of prion formation. The implication is that template-based protein folding may represent an inherent feature of neuropathogenic proteins that extends to retroviral Envs.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/1742-4690-7-93" target="_blank" rel="noreferrer noopener">10.1186/1742-4690-7-93</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Animals
Cell Line
Department of Integrative Medical Sciences
env/*metabolism
Experimental/*virology
Gene Products
Helper Viruses/metabolism/pathogenicity/*physiology
Leukemia
Leukemia Virus
Li Ying
Lynch William P
Mice
Motor Neuron Disease/*virology
Murine/metabolism/pathogenicity/*physiology
NEOMED College of Medicine
Neural Stem Cells/*virology
Protein Binding
Protein Folding
Protein Subunits/metabolism
Retroviridae Infections/*virology
Retrovirology
Tumor Virus Infections/*virology
Virulence
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1166/jbn.2013.1598" target="_blank" rel="noreferrer noopener">http://doi.org/10.1166/jbn.2013.1598</a>
Pages
1029–1040
Issue
6
Volume
9
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Antitumor efficacy and tolerability of systemically administered gallium acetylacetonate-loaded gelucire-stabilized nanoparticles.
Publisher
An entity responsible for making the resource available
Journal of biomedical nanotechnology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-06
Subject
The topic of the resource
*Lethal Dose 50; Adenocarcinoma/*drug therapy/pathology; Animals; Antineoplastic Agents/administration & dosage/pharmacokinetics/toxicity; Cell Line; Dose-Response Relationship; Drug; Drug Stability; Drug Tolerance; Gallium/*administration & dosage/pharmacokinetics/*toxicity; Humans; Metabolic Clearance Rate; Mice; Nanocapsules/*administration & dosage/chemistry/*toxicity; Nude; Organ Specificity; Tissue Distribution; Treatment Outcome; Triglycerides/chemistry; Tumor
Creator
An entity primarily responsible for making the resource
Wehrung Daniel; Bi Lipeng; Geldenhuys Werner J; Oyewumi Moses O
Description
An account of the resource
The widespread clinical success with most gallium compounds in cancer therapy is markedly hampered by lack of tumor specific accumulation, poor tumor permeability and undesirable toxicity to healthy tissues. The aim of this work was to investigate for the first time antitumor mechanism of a new gallium compound (gallium acetylacetonate; GaAcAc) while assessing effectiveness of gelucire-stabilized nanoparticles (NPs) for potential application in gallium-based lung cancer therapy. NPs loaded with GaAcAc (Ga-NPs) were prepared using mixtures of cetyl alcohol with Gelucire 44/14 (Ga-NP-1) or Gelucire 53/13 (Ga-NP-2) as matrix materials. Of special note from this work is the direct evidence of involvement of microtubule disruption in antitumor effects of GaAcAc on human lung adenocarcinoma (A549). In-vivo tolerability studies were based on plasma ALT, creatinine levels and histopathological examination of tissues. The superior in-vivo antitumor efficacy of Ga-NPs over GaAcAc was depicted in marked reduction of tumor weight and tumor volume as well as histological assessment of excised tumors. Compared to free GaAcAc, Ga-NPs showed a 3-fold increase in tumor-to-blood gallium concentrations with minimized overall exposure to healthy tissues. Overall, enhancement of antitumor effects of GaAcAc by gelucire-stabilized NPs coupled with reduced exposure of healthy tissues to gallium would likely ensure desired therapeutic outcomes and safety of gallium-based cancer treatment.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1166/jbn.2013.1598" target="_blank" rel="noreferrer noopener">10.1166/jbn.2013.1598</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lethal Dose 50
2013
Adenocarcinoma/*drug therapy/pathology
Animals
Antineoplastic Agents/administration & dosage/pharmacokinetics/toxicity
Bi Lipeng
Cell Line
Department of Pharmaceutical Sciences
Dose-Response Relationship
Drug
Drug Stability
Drug Tolerance
Gallium/*administration & dosage/pharmacokinetics/*toxicity
Geldenhuys Werner J
Humans
Journal of biomedical nanotechnology
Metabolic Clearance Rate
Mice
Nanocapsules/*administration & dosage/chemistry/*toxicity
NEOMED College of Pharmacy
Nude
Organ Specificity
Oyewumi Moses O
Tissue Distribution
Treatment Outcome
Triglycerides/chemistry
Tumor
Wehrung Daniel
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1166/jbn.2012.1361" target="_blank" rel="noreferrer noopener">http://doi.org/10.1166/jbn.2012.1361</a>
Pages
161–171
Issue
1
Volume
8
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Antitumor effect of novel gallium compounds and efficacy of nanoparticle-mediated gallium delivery in lung cancer.
Publisher
An entity responsible for making the resource available
Journal of biomedical nanotechnology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-02
Subject
The topic of the resource
Antineoplastic Agents/*administration & dosage/chemistry/pharmacokinetics; Biocompatible Materials/administration & dosage/chemistry/pharmacokinetics; Cell Line; Cell Survival/drug effects; Coordination Complexes/*administration & dosage/chemistry/pharmacokinetics; Drug Carriers/administration & dosage/chemistry; Drug Stability; Endocytosis/drug effects; Gallium/*administration & dosage/chemistry/pharmacokinetics; Hemolysis/drug effects; Humans; Lung Neoplasms/*drug therapy/metabolism; Materials Testing; Membrane Potential; Mitochondrial/drug effects; Nanoparticles/*administration & dosage/chemistry; Particle Size; Platelet Aggregation/drug effects; Reactive Oxygen Species/metabolism; Transferrin/chemistry/pharmacology; Tumor
Creator
An entity primarily responsible for making the resource
Wehrung Daniel; Oyewumi Moses O
Description
An account of the resource
The widespread application of gallium (Ga) in cancer therapy has been greatly hampered by lack of specificity resulting in poor tumor accumulation and retention. To address the challenge, two lipophilic gallium (III) compounds (gallium hexanedione; GaH and gallium acetylacetonate; GaAcAc) were synthesized and antitumor studies were conducted in human lung adenocarcinoma (A549) cells. Nanoparticles (NPs) containing various concentrations of the Ga compounds were prepared using a binary mixture of Gelucire 44/14 and cetyl alcohol as matrix materials. NPs were characterized based on size, morphology, stability and biocompatibility. Antitumor effects of free or NP-loaded Ga compounds were investigated based on cell viability, production of reactive oxygen species and reduction of mitochondrial potential. Compared to free Ga compounds, cytotoxicity of NP-loaded Ga (5-150 microg/ml) was less dependent on concentration and incubation time (exposure) with A549 cells. NP-mediated delivery (5-150 microg Ga/ml) enhanced antitumor effects of Ga compounds and the effect was pronounced at: (i) shorter incubation times; and (ii) at low concentrations of gallium (approximately 50 microg/ml) (p \textless 0.0006). Additional studies showed that
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1166/jbn.2012.1361" target="_blank" rel="noreferrer noopener">10.1166/jbn.2012.1361</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Antineoplastic Agents/*administration & dosage/chemistry/pharmacokinetics
Biocompatible Materials/administration & dosage/chemistry/pharmacokinetics
Cell Line
Cell Survival/drug effects
Coordination Complexes/*administration & dosage/chemistry/pharmacokinetics
Department of Pharmaceutical Sciences
Drug Carriers/administration & dosage/chemistry
Drug Stability
Endocytosis/drug effects
Gallium/*administration & dosage/chemistry/pharmacokinetics
Hemolysis/drug effects
Humans
Journal of biomedical nanotechnology
Lung Neoplasms/*drug therapy/metabolism
Materials Testing
Membrane Potential
Mitochondrial/drug effects
Nanoparticles/*administration & dosage/chemistry
NEOMED College of Pharmacy
Oyewumi Moses O
Particle Size
Platelet Aggregation/drug effects
Reactive Oxygen Species/metabolism
Transferrin/chemistry/pharmacology
Tumor
Wehrung Daniel
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2017/3613505" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2017/3613505</a>
Pages
3613505–3613505
Volume
2017
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
LEAPS Vaccine Incorporating HER-2/neu Epitope Elicits Protection That Prevents and Limits Tumor Growth and Spread of Breast Cancer in a Mouse Model.
Publisher
An entity responsible for making the resource available
Journal of immunology research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
*Cancer Vaccines/genetics/immunology/therapeutic use; Animal; Animals; Breast Neoplasms/genetics/immunology/prevention & control/therapy; CD8-Positive T-Lymphocytes/immunology; Cell Line; Cytotoxic/immunology; Disease Models; Disease Progression; Epitopes; erbB-2; Experimental/immunology/pathology/*prevention & control/*therapy; Female; Genes; Immunoglobulin G/blood; Inbred BALB C; Mammary Neoplasms; Mice; Neoplasm Metastasis/prevention & control; Proof of Concept Study; T-Lymphocyte/immunology; T-Lymphocytes; Tumor
Creator
An entity primarily responsible for making the resource
Rosenthal Ken S; Stone Sarah; Koski Gary; Zimmerman Daniel H
Description
An account of the resource
The prototype J-LEAPS T cell vaccine for HER-2/neu breast cancer (J-HER) consists of the murine HER-2/neu66-74 H-2(d) CD8 T cell epitope covalently attached through a triglycine linker to the J-immune cell binding ligand (ICBL) (human beta2 microglobulin38-50 peptide). The J-ICBL was chosen for its potential to promote Th1/Tc1 responses. In this proof-of-concept study, the ability of J-HER to prevent or treat cancer was tested in the TUBO cell-challenged BALB/c mouse model for HER-2/neu-expressing tumors. The J-HER vaccine was administered as an emulsion in Montanide ISA-51 without the need for a more potent adjuvant. When administered as a prophylactic vaccination before tumor challenge, J-HER protected against tumor development for at least 48 days. Despite eliciting protection, antibody production in J-HER-immunized, TUBO-challenged mice was less than that in unimmunized mice. More importantly, therapeutic administration of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2017/3613505" target="_blank" rel="noreferrer noopener">10.1155/2017/3613505</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cancer Vaccines/genetics/immunology/therapeutic use
2017
Animal
Animals
Breast Neoplasms/genetics/immunology/prevention & control/therapy
CD8-Positive T-Lymphocytes/immunology
Cell Line
Cytotoxic/immunology
Disease Models
Disease Progression
Epitopes
erbB-2
Experimental/immunology/pathology/*prevention & control/*therapy
Female
Genes
Immunoglobulin G/blood
Inbred BALB C
Journal of immunology research
Koski Gary
Mammary Neoplasms
Mice
Neoplasm Metastasis/prevention & control
Proof of Concept Study
Rosenthal Ken S
Stone Sarah
T-Lymphocyte/immunology
T-Lymphocytes
Tumor
Zimmerman Daniel H
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00449.2015</a>
Pages
H20–28
Issue
1
Volume
310
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
alpha Subunit/metabolism; Amino Acids; Animal; Animals; Apoptosis/drug effects; Cardiotonic Agents/*pharmacology; Cell Hypoxia; Cell Line; CXCR4/deficiency/genetics/*metabolism; Dicarboxylic/*pharmacology; Disease Models; Enzyme Inhibitors/pharmacology; hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism; Inbred C57BL; Knockout; Left/*drug effects; Mice; myocardial infarction; Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology; Myocardium/*metabolism/pathology; Rats; Receptors; Recovery of Function; Signal Transduction/drug effects; stem cells; Stem Cells/drug effects/metabolism; Stroke Volume/drug effects; Time Factors; Up-Regulation; Ventricular Function
Creator
An entity primarily responsible for making the resource
Mayorga Mari; Kiedrowski Matthew; Shamhart Patricia; Forudi Farhad; Weber Kristal; Chilian William M; Penn Marc S; Dong Feng
Description
An account of the resource
The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to engage the SDF-1:CXCR4 axis and improve cardiac repair. The effects of the hypoxia inducible factor (HIF) hydroxylase inhibitor dimethyloxalylglycine (DMOG) on CXCR4 expression was tested on H9c2 cells. In mice a myocardial infarction (MI) was produced in CM-CXCR4 null and wild-type controls. Mice were randomized to receive injection of DMOG (DMOG group) or saline (Saline group) into the border zone after MI. Protein and mRNA expression of CM-CXCR4 were quantified. Echocardiography was used to assess cardiac function. During hypoxia, DMOG treatment increased CXCR4 expression of H9c2 cells by 29 and 42% at 15 and 24 h, respectively. In vivo DMOG treatment increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00449.2015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
alpha Subunit/metabolism
American journal of physiology. Heart and circulatory physiology
Amino Acids
Animal
Animals
Apoptosis/drug effects
Cardiotonic Agents/*pharmacology
Cell Hypoxia
Cell Line
Chilian William M
CXCR4/deficiency/genetics/*metabolism
Department of Integrative Medical Sciences
Dicarboxylic/*pharmacology
Disease Models
Dong Feng
Enzyme Inhibitors/pharmacology
Forudi Farhad
hypoxia
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism
Inbred C57BL
Kiedrowski Matthew
Knockout
Left/*drug effects
Mayorga Mari
Mice
myocardial infarction
Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Penn Marc S
Rats
Receptors
Recovery of Function
Shamhart Patricia
Signal Transduction/drug effects
stem cells
Stem Cells/drug effects/metabolism
Stroke Volume/drug effects
Time Factors
Up-Regulation
Ventricular Function
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpgi.00207.2004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00207.2004</a>
Pages
G685–695
Issue
4
Volume
288
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Cytokine regulation of human sterol 12alpha-hydroxylase (CYP8B1) gene.
Publisher
An entity responsible for making the resource available
American journal of physiology. Gastrointestinal and liver physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-04
Subject
The topic of the resource
Cell Line; Chenodeoxycholic Acid/pharmacology; Chromosome Mapping; DNA-Binding Proteins/genetics/metabolism; Enzyme Inhibitors/pharmacology; Gene Expression Regulation/*drug effects; Genetic/drug effects; Genetic/physiology; Hepatocyte Nuclear Factor 4; Hepatocytes/metabolism; Humans; Interleukin-1/*pharmacology; MAP Kinase Signaling System/drug effects/physiology; Messenger/antagonists & inhibitors; Mitogen-Activated Protein Kinase 8/metabolism; Mitogen-Activated Protein Kinases/antagonists & inhibitors; Phosphoproteins/genetics/metabolism; Phosphorylation; Promoter Regions; Response Elements/genetics; RNA; Steroid 12-alpha-Hydroxylase/antagonists & inhibitors/*genetics; Transcription; Transcription Factors/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Jahan Asmeen; Chiang John Y L
Description
An account of the resource
Sterol 12alpha-hydroxylase (CYP8B1) catalyzes cholic acid synthesis in the liver and is feedback inhibited by bile acids. In addition to activating farnesoid X receptor (nuclear receptor subfamily 1H4), bile acids also induce inflammatory cytokines in hepatocytes. The objective of this study was to investigate the mechanism by which inflammatory cytokines inhibit human CYP8B1 gene transcription. Real-time PCR assays revealed that both chenodeoxycholic acid (CDCA) and interleukin-1beta (IL-1beta) markedly reduced CYP8B1, cholesterol 7alpha-hydroxylase CYP7A1 and hepatic nuclear factor 4alpha (HNF4alpha) mRNA expression levels in human primary hepatocytes. However, CDCA induced, but
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpgi.00207.2004" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00207.2004</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2005
American journal of physiology. Gastrointestinal and liver physiology
Cell Line
Chenodeoxycholic Acid/pharmacology
Chiang John Y L
Chromosome Mapping
Department of Integrative Medical Sciences
DNA-Binding Proteins/genetics/metabolism
Enzyme Inhibitors/pharmacology
Gene Expression Regulation/*drug effects
Genetic/drug effects
Genetic/physiology
Hepatocyte Nuclear Factor 4
Hepatocytes/metabolism
Humans
Interleukin-1/*pharmacology
Jahan Asmeen
MAP Kinase Signaling System/drug effects/physiology
Messenger/antagonists & inhibitors
Mitogen-Activated Protein Kinase 8/metabolism
Mitogen-Activated Protein Kinases/antagonists & inhibitors
NEOMED College of Medicine
Phosphoproteins/genetics/metabolism
Phosphorylation
Promoter Regions
Response Elements/genetics
RNA
Steroid 12-alpha-Hydroxylase/antagonists & inhibitors/*genetics
Transcription
Transcription Factors/genetics/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.03156-15</a>
Pages
3385–3399
Issue
7
Volume
90
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Ecotropic Murine Leukemia Virus Infection of Glial Progenitors Interferes with Oligodendrocyte Differentiation: Implications for Neurovirulence.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
3T3 Cells; Animals; Cell Line; Cell Proliferation; Cell Survival; env/biosynthesis; Female; Gene Products; Leukemia Virus; Male; Mice; Motor Neuron Disease/*virology; Murine/*pathogenicity; Neural Stem Cells/*virology; Neurogenesis/*physiology; Neuroglia/*virology; Oligodendroglia/cytology/virology; Retroviridae Infections/*complications; Transgenic
Creator
An entity primarily responsible for making the resource
Li Ying; Dunphy Jaclyn M; Pedraza Carlos E; Lynch Connor R; Cardona Sandra M; Macklin Wendy B; Lynch William P
Description
An account of the resource
UNLABELLED: Certain murine leukemia viruses (MLVs) are capable of inducing fatal progressive spongiform motor neuron disease in mice that is largely mediated by viral Env glycoprotein expression within central nervous system (CNS) glia. While the etiologic mechanisms and the glial subtypes involved remain unresolved, infection of NG2 glia was recently observed to correlate spatially and temporally with altered neuronal physiology and spongiogenesis. Since one role of NG2 cells is to serve as oligodendrocyte (OL) progenitor cells (OPCs), we examined here whether their infection by neurovirulent (FrCasE) or nonneurovirulent (Fr57E) ecotropic MLVs influenced their viability and/or differentiation. Here, we demonstrate that OPCs, but not OLs, are major CNS targets of both FrCasE and Fr57E. We also show that MLV infection of neural progenitor cells (NPCs) in culture did not affect survival, proliferation, or OPC progenitor marker expression but suppressed certain glial differentiation markers. Assessment of glial differentiation in vivo using transplanted transgenic NPCs showed that, while MLVs did not affect cellular engraftment or survival, they did inhibit OL differentiation, irrespective of MLV neurovirulence. In addition, in chimeric brains, where FrCasE-infected NPC transplants caused neurodegeneration, the transplanted NPCs proliferated. These results suggest that MLV infection is not directly cytotoxic to OPCs but rather acts to interfere with OL differentiation. Since both FrCasE and Fr57E viruses restrict OL differentiation but only FrCasE induces overt neurodegeneration, restriction of OL maturation alone cannot account for neuropathogenesis. Instead neurodegeneration may involve a two-hit scenario where interference with OPC differentiation combined with glial Env-induced neuronal hyperexcitability precipitates disease. IMPORTANCE: A variety of human and animal retroviruses are capable of causing central nervous system (CNS) neurodegeneration manifested as motor and cognitive deficits. These retroviruses infect a variety of CNS cell types; however, the specific role each cell type plays in neuropathogenesis remains to be established. The NG2 glia, whose CNS functions are only now emerging, are a newly appreciated viral target in murine leukemia virus (MLV)-induced neurodegeneration. Since one role of NG2 glia is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by the neurovirulent MLV FrCasE contributed to neurodegeneration by affecting OPC viability and/or development. Our results show that both neurovirulent and nonneurovirulent MLVs interfere with oligodendrocyte differentiation. Thus, NG2 glial infection could contribute to neurodegeneration by preventing myelin formation and/or repair and by suspending OPCs in a state of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effects on other glial subtypes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">10.1128/JVI.03156-15</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
3T3 Cells
Animals
Cardona Sandra M
Cell Line
Cell Proliferation
Cell Survival
Department of Integrative Medical Sciences
Dunphy Jaclyn M
env/biosynthesis
Female
Gene Products
Journal of virology
Leukemia Virus
Li Ying
Lynch Connor R
Lynch William P
Macklin Wendy B
Male
Mice
Motor Neuron Disease/*virology
Murine/*pathogenicity
NEOMED College of Medicine
Neural Stem Cells/*virology
Neurogenesis/*physiology
Neuroglia/*virology
Oligodendroglia/cytology/virology
Pedraza Carlos E
Retroviridae Infections/*complications
Transgenic
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.02210-10" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.02210-10</a>
Pages
2060–2078
Issue
5
Volume
85
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Retrovirus-induced spongiform neurodegeneration is mediated by unique central nervous system viral targeting and expression of env alone.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-03
Subject
The topic of the resource
Animals; Cell Line; Friend murine leukemia virus/genetics/metabolism; Humans; Leukemia Virus; Mice; Murine/genetics/*metabolism/pathogenicity; Nerve Degeneration; Neural Stem Cells/pathology/virology; Neurodegenerative Diseases/pathology/*virology; Retroviridae Infections/pathology/*virology; Viral Envelope Proteins/genetics/*metabolism; Virulence
Creator
An entity primarily responsible for making the resource
Li Ying; Cardona Sandra M; Traister Russell S; Lynch William P
Description
An account of the resource
Certain murine leukemia viruses (MLVs) can induce progressive noninflammatory spongiform neurodegeneration similar to that caused by prions. The primary MLV determinants responsible have been mapped to within the env gene; however, it has remained unclear how env mediates disease, whether non-Env viral components are required, and what central nervous system (CNS) cells constitute the critical CNS targets. To address these questions, we examined the effect of transplanting engraftable C17.2 neural stem cells engineered to pseudotype, disseminate, and trans-complement neurovirulent (CasBrE, CasE, and CasES) or non-neurovirulent (Friend and SFF-FE) env sequences (SU or SU/TM) within the CNS using either the "non-neurovirulent" amphotropic helper virus, 4070A, or pgag-polgpt (a nonpackaged vector encoding Gag-Pol). These studies revealed that acute
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.02210-10" target="_blank" rel="noreferrer noopener">10.1128/JVI.02210-10</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
Animals
Cardona Sandra M
Cell Line
Department of Integrative Medical Sciences
Friend murine leukemia virus/genetics/metabolism
Humans
Journal of virology
Leukemia Virus
Li Ying
Lynch William P
Mice
Murine/genetics/*metabolism/pathogenicity
NEOMED College of Medicine
Nerve Degeneration
Neural Stem Cells/pathology/virology
Neurodegenerative Diseases/pathology/*virology
Retroviridae Infections/pathology/*virology
Traister Russell S
Viral Envelope Proteins/genetics/*metabolism
Virulence
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1124/dmd.108.025155" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/dmd.108.025155</a>
Pages
469–478
Issue
3
Volume
37
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mechanism of vitamin D receptor inhibition of cholesterol 7alpha-hydroxylase gene transcription in human hepatocytes.
Publisher
An entity responsible for making the resource available
Drug metabolism and disposition: the biological fate of chemicals
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-03
Subject
The topic of the resource
Base Sequence; Calcitriol/drug effects/genetics/*physiology; Cell Line; Cells; Cholesterol 7-alpha-Hydroxylase/*genetics; Cultured; DNA Primers; Electrophoretic Mobility Shift Assay; Gene Knockdown Techniques; Genetic/*physiology; Hepatocytes/*drug effects/enzymology; Humans; Immunoprecipitation; Lithocholic Acid/pharmacology; Messenger/genetics; Polymerase Chain Reaction; Receptors; RNA; Small Interfering; Transcription; Tumor; Two-Hybrid System Techniques
Creator
An entity primarily responsible for making the resource
Han Shuxin; Chiang John Y L
Description
An account of the resource
Lithocholic acid (LCA) is a potent endogenous vitamin D receptor (VDR) ligand. In cholestasis, LCA levels increase in the liver and intestine. The objective of this study is to test the hypothesis that VDR plays a role in inhibiting cholesterol 7alpha-hydroxylase (CYP7A1) gene expression and bile acid synthesis in human hepatocytes. Immunoblot analysis has detected VDR proteins in the nucleus of the human hepatoma cell line HepG2 and human primary hepatocytes. 1alpha, 25-Dihydroxy-vitamin D(3) or LCA acetate-activated VDR inhibited CYP7A1 mRNA expression and bile acid synthesis, whereas small interfering RNA to VDR completely abrogated VDR inhibition of CYP7A1 mRNA expression in HepG2 cells. Electrophoretic mobility shift assay and mutagenesis analyses have identified the negative VDR response elements that bind VDR/retinoid X receptor alpha in the human CYP7A1 promoter. Mammalian two-hybrid, coimmunoprecipitation, glutathione
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/dmd.108.025155" target="_blank" rel="noreferrer noopener">10.1124/dmd.108.025155</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2009
Base Sequence
Calcitriol/drug effects/genetics/*physiology
Cell Line
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics
Cultured
Department of Integrative Medical Sciences
DNA Primers
Drug metabolism and disposition: the biological fate of chemicals
Electrophoretic Mobility Shift Assay
Gene Knockdown Techniques
Genetic/*physiology
Han Shuxin
Hepatocytes/*drug effects/enzymology
Humans
Immunoprecipitation
Lithocholic Acid/pharmacology
Messenger/genetics
NEOMED College of Medicine
Polymerase Chain Reaction
Receptors
RNA
Small Interfering
Transcription
Tumor
Two-Hybrid System Techniques
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1124/dmd.105.007575" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/dmd.105.007575</a>
Pages
756–764
Issue
5
Volume
34
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Rifampicin induction of CYP3A4 requires pregnane X receptor cross talk with hepatocyte nuclear factor 4alpha and coactivators, and suppression of small heterodimer partner gene expression.
Publisher
An entity responsible for making the resource available
Drug metabolism and disposition: the biological fate of chemicals
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-05
Subject
The topic of the resource
Antibiotics; Antitubercular/*pharmacology; Blotting; Cell Line; Chromatin/metabolism; Cytochrome P-450 CYP3A; Cytochrome P-450 Enzyme System/*biosynthesis; Cytoplasmic and Nuclear/*biosynthesis/*drug effects/genetics; Electrophoretic Mobility Shift Assay; Enzyme Induction/drug effects; Glutathione Transferase/metabolism; Hepatocyte Nuclear Factor 4/genetics/*metabolism; Hepatocytes/drug effects/metabolism; Humans; Immunoprecipitation; Messenger/biosynthesis; Plasmids/genetics; Pregnane X Receptor; Receptor Cross-Talk/drug effects; Receptors; Reverse Transcriptase Polymerase Chain Reaction; Rifampin/*pharmacology; RNA; Steroid/*drug effects/genetics; Transfection; Tumor; Western
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chiang John Y L
Description
An account of the resource
Bile acids and drugs activate pregnane X receptor (PXR) to induce CYP3A4, which is the predominant cytochrome P450 enzyme expressed in the liver and intestine and plays a critical role in detoxifying bile acids and drugs, and protecting against cholestasis. The aim of this study is to investigate the molecular mechanism of PXR cross talk with other nuclear receptors and coactivators in regulating human CYP3A4 gene transcription. Rifampicin dose dependently induced the CYP3A4 but inhibited small heterodimer partner (SHP) mRNA expression levels in primary human hepatocytes. Rifampicin strongly stimulated PXR and hepatocyte nuclear factor 4alpha (HNF4alpha) interaction, and CYP3A4 reporter activity, which was further stimulated by peroxisome proliferators-activated receptorgamma co-activator 1alpha (PGC-1alpha) and steroid receptor coactivator-1 (SRC-1) but inhibited by SHP. Mutation of the putative HNF4alpha binding site in the distal xenobiotic responsive element module did not affect CYP3A4 basal promoter activity and synergistic stimulation by PXR and HNF4alpha. Chromatin immunoprecipitation assays revealed that rifampicin-activated PXR recruited HNF4alpha and SRC-1 to the CYP3A4 chromatin. On the other hand, SHP reduced PXR recruitment of HNF4alpha and SRC-1 to the CYP3A4 chromatin. The human SHP promoter was stimulated by HNF4alpha and PGC-1alpha. Upon activation by rifampicin, PXR inhibited SHP promoter activity. Results suggest that PXR strongly induces CYP3A4 gene transcription by interacting with HNF4alpha, SRC-1, and PGC-1alpha. PXR concomitantly inhibits SHP gene transcription and maximizes the PXR induction of the CYP3A4 gene in human livers. Drugs targeted to PXR may be developed for treating cholestatic liver diseases induced by bile acids and drugs.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/dmd.105.007575" target="_blank" rel="noreferrer noopener">10.1124/dmd.105.007575</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2006
Antibiotics
Antitubercular/*pharmacology
Blotting
Cell Line
Chiang John Y L
Chromatin/metabolism
Cytochrome P-450 CYP3A
Cytochrome P-450 Enzyme System/*biosynthesis
Cytoplasmic and Nuclear/*biosynthesis/*drug effects/genetics
Department of Integrative Medical Sciences
Drug metabolism and disposition: the biological fate of chemicals
Electrophoretic Mobility Shift Assay
Enzyme Induction/drug effects
Glutathione Transferase/metabolism
Hepatocyte Nuclear Factor 4/genetics/*metabolism
Hepatocytes/drug effects/metabolism
Humans
Immunoprecipitation
Li Tiangang
Messenger/biosynthesis
NEOMED College of Medicine
Plasmids/genetics
Pregnane X Receptor
Receptor Cross-Talk/drug effects
Receptors
Reverse Transcriptase Polymerase Chain Reaction
Rifampin/*pharmacology
RNA
Steroid/*drug effects/genetics
Transfection
Tumor
Western
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1113/JP272796" target="_blank" rel="noreferrer noopener">http://doi.org/10.1113/JP272796</a>
Pages
7341–7360
Issue
24
Volume
594
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Hyperammonaemia-induced skeletal muscle mitochondrial dysfunction results in cataplerosis and oxidative stress.
Publisher
An entity responsible for making the resource available
The Journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*ammonia; *ATP; *cellular respiration; *cirrhosis; *mitochondria; *Oxidative Stress; *portacaval anastamosis; *reactive oxygen species; *skeletal muscle; Adenosine Triphosphate/metabolism; Aged; Animals; Cell Line; Cell Respiration; Creatine Kinase/metabolism; Female; Humans; Hyperammonemia/*metabolism; Liver Cirrhosis/metabolism; Male; Middle Aged; Mitochondria; Muscle; Muscle/*metabolism; Myosin Heavy Chains/metabolism; NAD/metabolism; Rats; Reactive Oxygen Species/metabolism; Skeletal/*metabolism; Sprague-Dawley; Thiobarbituric Acid Reactive Substances/metabolism
Creator
An entity primarily responsible for making the resource
Davuluri Gangarao; Allawy Allawy; Thapaliya Samjhana; Rennison Julie H; Singh Dharmvir; Kumar Avinash; Sandlers Yana; Van Wagoner David R; Flask Chris A; Hoppel Charles; Kasumov Takhar; Dasarathy Srinivasan
Description
An account of the resource
KEY POINTS: Hyperammonaemia occurs in hepatic, cardiac and pulmonary diseases with increased muscle concentration of ammonia. We found that ammonia results in reduced skeletal muscle mitochondrial respiration, electron transport chain complex I dysfunction, as well as lower NAD(+) /NADH ratio and ATP content. During hyperammonaemia, leak of electrons from complex III results in oxidative modification of proteins and lipids. Tricarboxylic acid cycle intermediates are decreased during hyperammonaemia, and providing a cell-permeable ester of alphaKG reversed the lower TCA cycle intermediate concentrations and increased ATP content. Our observations have high clinical relevance given the potential for novel approaches to reverse skeletal muscle ammonia toxicity by targeting the TCA cycle intermediates and mitochondrial ROS. ABSTRACT: Ammonia is a cytotoxic metabolite that is removed primarily by hepatic ureagenesis in humans. Hyperammonaemia occurs in advanced hepatic, cardiac and pulmonary disease, and in urea cycle enzyme deficiencies. Increased skeletal muscle ammonia uptake and metabolism are the major mechanism of non-hepatic ammonia disposal. Non-hepatic ammonia disposal occurs in the mitochondria via glutamate synthesis from alpha-ketoglutarate resulting in cataplerosis. We show skeletal muscle mitochondrial dysfunction during hyperammonaemia in a comprehensive array of human, rodent and cellular models. ATP synthesis, oxygen consumption, generation of reactive oxygen species with oxidative stress, and tricarboxylic acid (TCA) cycle intermediates were quantified. ATP content was lower in the skeletal muscle from cirrhotic patients, hyperammonaemic portacaval anastomosis rat, and C2C12 myotubes compared to appropriate controls. Hyperammonaemia in C2C12 myotubes resulted in impaired intact cell respiration, reduced complex I/NADH oxidase activity and electron leak occurring at complex III of the electron transport chain. Consistently, lower NAD(+) /NADH ratio was observed during hyperammonaemia with reduced TCA cycle intermediates compared to controls. Generation of reactive oxygen species resulted in increased content of skeletal muscle carbonylated proteins and thiobarbituric acid reactive substances during hyperammonaemia. A cell-permeable ester of alpha-ketoglutarate reversed the low TCA cycle intermediates and ATP content in myotubes during hyperammonaemia. However, the mitochondrial antioxidant MitoTEMPO did not reverse the lower ATP content during hyperammonaemia. We provide for the first time evidence that skeletal muscle hyperammonaemia results in mitochondrial dysfunction and oxidative stress. Use of anaplerotic substrates to reverse ammonia-induced mitochondrial dysfunction is a novel therapeutic approach.
Identifier
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<a href="http://doi.org/10.1113/JP272796" target="_blank" rel="noreferrer noopener">10.1113/JP272796</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*ammonia
*ATP
*cellular respiration
*cirrhosis
*Mitochondria
*Oxidative Stress
*portacaval anastamosis
*Reactive oxygen species
*skeletal muscle
2016
Adenosine Triphosphate/metabolism
Aged
Allawy Allawy
Animals
Cell Line
Cell Respiration
Creatine Kinase/metabolism
Dasarathy Srinivasan
Davuluri Gangarao
Department of Pharmaceutical Sciences
Female
Flask Chris A
Hoppel Charles
Humans
Hyperammonemia/*metabolism
Kasumov Takhar
Kumar Avinash
Liver Cirrhosis/metabolism
Male
Middle Aged
Mitochondria
Muscle
Muscle/*metabolism
Myosin Heavy Chains/metabolism
NAD/metabolism
NEOMED College of Pharmacy
Rats
Reactive Oxygen Species/metabolism
Rennison Julie H
Sandlers Yana
Singh Dharmvir
Skeletal/*metabolism
Sprague-Dawley
Thapaliya Samjhana
The Journal of physiology
Thiobarbituric Acid Reactive Substances/metabolism
Van Wagoner David R
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1099/0022-1317-70-4-857" target="_blank" rel="noreferrer noopener">http://doi.org/10.1099/0022-1317-70-4-857</a>
Pages
857–867
Volume
70 ( Pt 4)
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mild acidic pH inhibition of the major pathway of herpes simplex virus entry into HEp-2 cells.
Publisher
An entity responsible for making the resource available
The Journal of general virology
Date
A point or period of time associated with an event in the lifecycle of the resource
1989
1989-04
Subject
The topic of the resource
Animals; Cell Line; Electron; Electrophoresis; Endocytosis; Glycoproteins/analysis; Glycosylation; Humans; Hydrogen-Ion Concentration; Microscopy; Polyacrylamide Gel; Simplexvirus/*physiology/ultrastructure; Temperature; Time Factors; Vero Cells; Viral Proteins/analysis/metabolism
Creator
An entity primarily responsible for making the resource
Rosenthal K S; Killius J; Hodnichak C M; Venetta T M; Gyurgyik L; Janiga K
Description
An account of the resource
Penetration of the KOS strain of herpes simplex virus type 1 (HSV-1) and the MS and 333 strains of herpes simplex virus type 2 (HSV-2) into HEp-2 cells at pH 6.3 was at least 100-fold less efficient than at pH 7.4. Penetration of two low passage clinical isolates was completely blocked at pH 6.3. The syncytium-forming
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1099/0022-1317-70-4-857" target="_blank" rel="noreferrer noopener">10.1099/0022-1317-70-4-857</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1989
Animals
Cell Line
Electron
Electrophoresis
Endocytosis
Glycoproteins/analysis
Glycosylation
Gyurgyik L
Hodnichak C M
Humans
Hydrogen-Ion Concentration
Janiga K
Killius J
Microscopy
Polyacrylamide Gel
Rosenthal K S
Simplexvirus/*physiology/ultrastructure
Temperature
The Journal of general virology
Time Factors
Venetta T M
Vero Cells
Viral Proteins/analysis/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1093/toxsci/kfw187" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfw187</a>
Pages
112–123
Issue
1
Volume
155
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pyrethroid Insecticides Directly Activate Microglia Through Interaction With Voltage-Gated Sodium Channels.
Publisher
An entity responsible for making the resource available
Toxicological sciences : an official journal of the Society of Toxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-01
Subject
The topic of the resource
*deltamethrin; *intracellular sodium.; *microglia; *neurodegeneration; *neuroinflammation; *permethrin; *pyrethroids; *tetrodotoxin; *tumor necrosis factor; *voltage-gated sodium channels; Animals; Cell Line; Dose-Response Relationship; Drug; Inbred C57BL; Insecticides/*toxicity; Ion Channel Gating/*drug effects; Mice; Microglia/*drug effects/metabolism; Pyrethrins/*toxicity; Sodium Channels/*drug effects; Transformed; Tumor Necrosis Factor-alpha/metabolism
Creator
An entity primarily responsible for making the resource
Hossain Muhammad M; Liu Jason; Richardson Jason R
Description
An account of the resource
Microglia are considered to be the resident immune cells of the central nervous system and contribute significantly to ongoing neuroinflammation in a variety of neurodegenerative diseases. Recently, we and others identified that voltage-gated sodium channels (VGSC) are present on microglia cells and contribute to excessive accumulation of intracellular Na(+ )and release of major pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha). Based on this finding and the fact that pyrethroid pesticides act on VGSC, we hypothesized that exposure of microglia to the pyrethroid pesticides, permethrin and deltamethrin, would activate microglia and increase the release of TNF-alpha. BV2 cells or primary microglia were treated with 0-5 microM deltamethrin or permethrin in the presence or absence of tetrodotoxin (TTX), a VGSC blocker for 24-48 h. Both pyrethroids caused a rapid Na(+ )influx and increased accumulation of intracellular sodium [(Na(+))i] in the microglia in a dose- and time-dependent manner, which was significantly reduced by TTX. Furthermore, deltamethrin and permethrin increased the release of TNF-alpha in a dose- and time-dependent manner, which was significantly reduced by pre-treatment of cells with TTX. These results demonstrate that pyrethroid pesticides may directly activate microglial cells through their interaction with microglial VGSC. Because neuroinflammation plays a key role in many neurodegenerative diseases, these data provide an additional mechanism by which exposure to pyrethroid insecticides may contribute to neurodegeneration.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/toxsci/kfw187" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfw187</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*deltamethrin
*intracellular sodium.
*Microglia
*neurodegeneration
*Neuroinflammation
*permethrin
*pyrethroids
*tetrodotoxin
*tumor necrosis factor
*Voltage-gated sodium channels
2017
Animals
Cell Line
Department of Pharmaceutical Sciences
Dose-Response Relationship
Drug
Hossain Muhammad M
Inbred C57BL
Insecticides/*toxicity
Ion Channel Gating/*drug effects
Liu Jason
Mice
Microglia/*drug effects/metabolism
NEOMED College of Pharmacy
Pyrethrins/*toxicity
Richardson Jason R
Sodium Channels/*drug effects
Toxicological sciences : an official journal of the Society of Toxicology
Transformed
Tumor Necrosis Factor-alpha/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1080/13550280600970417" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/13550280600970417</a>
Pages
365–374
Issue
5
Volume
12
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Innate and adaptive host response during the initial phase of herpes simplex virus encephalitis in the neonatal mouse.
Publisher
An entity responsible for making the resource available
Journal of neurovirology
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-10
Subject
The topic of the resource
*Immunity; Active; Animal; Animals; B-Lymphocytes/immunology; Brain/pathology/*virology; Cell Line; Disease Models; Encephalitis; Herpes Simplex/*immunology; Innate; Mice; Microglia/pathology/virology; Newborn; Simplexvirus/*isolation & purification/physiology; T-Lymphocytes/immunology; Virus Replication
Creator
An entity primarily responsible for making the resource
Kumaraswamy Guttalu K; Fu Ming Ming; Docherty John J
Description
An account of the resource
To study early events of neonatal herpes simplex virus (HSV) encephalitis and its sequelae, the authors induced a controlled infection in the brains of mice using HSVgH, a genetically modified Disabled Infective Single Cycle virus. Neonatal Balb/C mice were infected with various amounts of HSVgH- virus by intracerebral injection. Results showed that the survival of infected mice was dependent on the amount of virus injected. Infection with 200,000 plaque forming units (pfu) of HSVgH-, virus resulted in 0% survival, whereas 25,000 pfu resulted in 75% survival. If the mice died, 98% of the deaths occurred between 3 and 7 days after infection. Replication competent virus was recovered from 20% of mice brains infected with 25,000 pfu of HSVgH-. Neutralizing antibodies were not detected 6 weeks post infection in sera of mice, which survived infection with 25,000 pfu of HSVgH-. LacZ histochemistry and immunoperoxidase staining using anti-HSV and anti- beta-galactosidase antibodies revealed that the infection was limited to the site of injection. Tissue destruction was observed at the site of inoculation 3 days post infection using cresyl violet staining. At 3 days post infection adjacent sections showed positive cells for viral antigens and apoptotic cells in the infected area. Immunoperoxidase staining using antibodies to surface markers showed microglial activation beginning on day 1 and astrocyte proliferation beginning on day 3 post infection. B and T lymphocytes were not detected on day 1 through 7 post infection. This controlled experimental HSV infection suggests a limited non-specific early host response in the neonate to HSV encephalitis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/13550280600970417" target="_blank" rel="noreferrer noopener">10.1080/13550280600970417</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Immunity
2006
Active
Animal
Animals
B-Lymphocytes/immunology
Brain/pathology/*virology
Cell Line
Disease Models
Docherty John J
Encephalitis
Fu Ming Ming
Herpes Simplex/*immunology
Innate
Journal of neurovirology
Kumaraswamy Guttalu K
Mice
Microglia/pathology/virology
Newborn
Simplexvirus/*isolation & purification/physiology
T-Lymphocytes/immunology
Virus Replication
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M513420200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M513420200</a>
Pages
10081–10088
Issue
15
Volume
281
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A Prospero-related homeodomain protein is a novel co-regulator of hepatocyte nuclear factor 4alpha that regulates the cholesterol 7alpha-hydroxylase gene.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-04
Subject
The topic of the resource
*Gene Expression Regulation; Aged; Amino Acid Motifs; Bile Acids and Salts/metabolism; Cell Line; Cell Nucleus/metabolism; Cells; Cholesterol 7-alpha-Hydroxylase/*chemistry/*genetics; Cultured/metabolism; Enzymologic; Female; Genes; Genetic; Gluconeogenesis; Glutathione Transferase/metabolism; Hepatocyte Nuclear Factor 4/metabolism/*physiology; Hepatocytes/metabolism; Homeodomain Proteins/metabolism/*physiology; Humans; Immunoprecipitation; Liver/metabolism; Luciferases/metabolism; Male; Messenger/metabolism; Middle Aged; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism; Plasmids/metabolism; Protein Structure; Reporter; Response Elements; Reverse Transcriptase Polymerase Chain Reaction; RNA; Small Interfering/metabolism; Tertiary; Time Factors; Transcription; Transcriptional Activation; Transfection; Tumor Suppressor Proteins; Two-Hybrid System Techniques
Creator
An entity primarily responsible for making the resource
Song Kwang-Hoon; Li Tiangang; Chiang John Y L
Description
An account of the resource
Prox1, an early specific marker for developing liver and pancreas in foregut endoderm has recently been shown to interact with alpha-fetoprotein transcription factor and repress cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription. Using a yeast two-hybrid assay, we found that Prox1 strongly and specifically interacted with hepatocyte nuclear factor (HNF)4alpha, an important transactivator of the human CYP7A1 gene in bile acid synthesis and phosphoenolpyruvate carboxykinase (PEPCK) gene in gluconeogenesis. A real time PCR assay detected Prox1 mRNA expression in human primary hepatocytes and HepG2 cells. Reporter assay, GST pull-down, co-immunoprecipitation, and yeast two-hybrid assays identified a specific interaction between the N-terminal LXXLL motif of Prox1 and the activation function 2 domain of HNF4alpha. Prox1 strongly inhibited HNF4alpha and peroxisome proliferators-activated receptor gamma coactivator-1alpha co-activation of the CYP7A1 and PEPCK genes. Knock down of the endogenous Prox1 by small interfering RNA resulted in significant increase of CYP7A1 and PEPCK mRNA expression and the rate of bile acid synthesis in HepG2 cells. These results suggest that Prox1 is a novel co-regulator of HNF4alpha that may play a key role in the regulation of bile acid synthesis and gluconeogenesis in the liver.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M513420200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M513420200</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2006
Aged
Amino Acid Motifs
Bile Acids and Salts/metabolism
Cell Line
Cell Nucleus/metabolism
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*chemistry/*genetics
Cultured/metabolism
Department of Integrative Medical Sciences
Enzymologic
Female
Genes
Genetic
Gluconeogenesis
Glutathione Transferase/metabolism
Hepatocyte Nuclear Factor 4/metabolism/*physiology
Hepatocytes/metabolism
Homeodomain Proteins/metabolism/*physiology
Humans
Immunoprecipitation
Li Tiangang
Liver/metabolism
Luciferases/metabolism
Male
Messenger/metabolism
Middle Aged
NEOMED College of Medicine
Phosphoenolpyruvate Carboxykinase (ATP)/metabolism
Plasmids/metabolism
Protein Structure
Reporter
Response Elements
Reverse Transcriptase Polymerase Chain Reaction
RNA
Small Interfering/metabolism
Song Kwang-Hoon
Tertiary
The Journal of biological chemistry
Time Factors
Transcription
Transcriptional Activation
Transfection
Tumor Suppressor Proteins
Two-Hybrid System Techniques
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M502751200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M502751200</a>
Pages
30517–30525
Issue
34
Volume
280
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Bcl-2 positively regulates Sox9-dependent chondrocyte gene expression by suppressing the MEK-ERK1/2 signaling pathway.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-08
Subject
The topic of the resource
*Gene Expression Regulation; Adenoviridae/genetics; Animals; Apoptosis; beta-Galactosidase/metabolism; Blotting; Butadienes/pharmacology; Caspase Inhibitors; Cell Differentiation; Cell Line; Chondrocytes/*metabolism; Collagen Type II/metabolism; Down-Regulation; Enzyme Inhibitors/pharmacology; Fibroblasts/metabolism; Fluorescence; Genetic; High Mobility Group Proteins/*metabolism; Lac Operon; Luciferases/metabolism; MAP Kinase Kinase Kinases/*metabolism; Messenger/metabolism; Microscopy; Mitogen-Activated Protein Kinase 1/*metabolism; Mitogen-Activated Protein Kinase 3/*metabolism; NF-kappa B/metabolism; Nitriles/pharmacology; Phenotype; Phosphorylation; Promoter Regions; Protein Kinase C-alpha; Protein Kinase C/antagonists & inhibitors; Proteoglycans/metabolism; Proto-Oncogene Proteins c-bcl-2/*metabolism; Rats; Reverse Transcriptase Polymerase Chain Reaction; RNA; Signal Transduction; Small Interfering/metabolism; SOX9 Transcription Factor; Sprague-Dawley; Time Factors; Transcription; Transcription Factors/*metabolism; Transfection; Western
Creator
An entity primarily responsible for making the resource
Yagi Rieko; McBurney Denise; Horton Walter E Jr
Description
An account of the resource
Bcl-2 is an anti-apoptotic protein that has recently been shown to regulate other cellular functions. We previously reported that Bcl-2 regulates chondrocyte matrix gene expression, independent of its anti-apoptotic function. Here, we further investigate this novel function of Bcl-2 and examine three intracellular signaling pathways likely to be associated with this function. The present study demonstrates that the activity of Sox9, a master transcription factor that regulates the gene expression of chondrocyte matrix proteins, is suppressed by Bcl-2 small interference RNA in the presence of caspase inhibitors. This effect was attenuated by prior exposure of chondrocytes to an adenoviral vector expressing sense Bcl-2. In addition, the down-regulation of Bcl-2, Sox9, and chondrocyte-specific gene expression by serum withdrawal in primary chondrocytes was reversed by expressing Bcl-2. Inhibition of the protein kinase C alpha and NFkappaB pathways had no effect on the maintenance of Sox9-dependent gene expression by Bcl-2. In contrast, whereas the MEK-ERK1/2 pathway negatively regulated the differentiated phenotype in wild type chondrocytes, inhibition of this pathway reversed the loss of differentiation markers and fibroblastic phenotype in Bcl-2-deficient chondrocytes. In conclusion, the present study identifies a specific signaling pathway, namely, MEK-ERK1/2, that is downstream of Bcl-2 in the regulation of Sox9-dependent chondrocyte gene expression and phenotype.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M502751200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M502751200</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2005
Adenoviridae/genetics
Animals
Apoptosis
beta-Galactosidase/metabolism
Blotting
Butadienes/pharmacology
Caspase Inhibitors
Cell Differentiation
Cell Line
Chondrocytes/*metabolism
Collagen Type II/metabolism
Department of Anatomy & Neurobiology
Down-Regulation
Enzyme Inhibitors/pharmacology
Fibroblasts/metabolism
Fluorescence
Genetic
High Mobility Group Proteins/*metabolism
Horton Walter E Jr
Lac Operon
Luciferases/metabolism
MAP Kinase Kinase Kinases/*metabolism
McBurney Denise
Messenger/metabolism
Microscopy
Mitogen-Activated Protein Kinase 1/*metabolism
Mitogen-Activated Protein Kinase 3/*metabolism
NEOMED College of Medicine
NF-kappa B/metabolism
Nitriles/pharmacology
Phenotype
Phosphorylation
Promoter Regions
Protein Kinase C-alpha
Protein Kinase C/antagonists & inhibitors
Proteoglycans/metabolism
Proto-Oncogene Proteins c-bcl-2/*metabolism
Rats
Reverse Transcriptase Polymerase Chain Reaction
RNA
Signal Transduction
Small Interfering/metabolism
SOX9 Transcription Factor
Sprague-Dawley
The Journal of biological chemistry
Time Factors
Transcription
Transcription Factors/*metabolism
Transfection
Western
Yagi Rieko
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M109.083899" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M109.083899</a>
Pages
3035–3043
Issue
5
Volume
285
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Identification of novel pathways that control farnesoid X receptor-mediated hypocholesterolemia.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-01
Subject
The topic of the resource
Absorption; Animals; Biological; Cell Line; Cholesterol/*metabolism; Class B/*genetics/metabolism; Coronary Disease/metabolism; Cytoplasmic and Nuclear/*metabolism; Glucose/metabolism; Hepatocyte Nuclear Factor 4/metabolism; Homeostasis; Humans; Lipoproteins/metabolism; Liver/metabolism; Mice; Models; Receptors; Scavenger Receptors
Creator
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Zhang Yanqiao; Yin Liya; Anderson Jody; Ma Huiyan; Gonzalez Frank J; Willson Timothy M; Edwards Peter A
Description
An account of the resource
Farnesoid X receptor (FXR) plays important regulatory roles in bile acid, lipoprotein, and glucose homeostasis. Here, we have utilized Fxr(-/-) mice and mice deficient in scavenger receptor class B type I (SR-BI), together with an
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M109.083899" target="_blank" rel="noreferrer noopener">10.1074/jbc.M109.083899</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Absorption
Anderson Jody
Animals
Biological
Cell Line
Cholesterol/*metabolism
Class B/*genetics/metabolism
Coronary Disease/metabolism
Cytoplasmic and Nuclear/*metabolism
Department of Integrative Medical Sciences
Edwards Peter A
Glucose/metabolism
Gonzalez Frank J
Hepatocyte Nuclear Factor 4/metabolism
Homeostasis
Humans
Lipoproteins/metabolism
Liver/metabolism
Ma Huiyan
Mice
Models
NEOMED College of Medicine
Receptors
Scavenger Receptors
The Journal of biological chemistry
Willson Timothy M
Yin Liya
Zhang Yanqiao
-
Text
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URL Address
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">http://doi.org/10.1053/j.gastro.2007.08.042</a>
Pages
1660–1669
Issue
5
Volume
133
Dublin Core
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Title
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A novel role of transforming growth factor beta1 in transcriptional repression of human cholesterol 7alpha-hydroxylase gene.
Publisher
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Gastroenterology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-11
Subject
The topic of the resource
Bile Acids and Salts/metabolism; Carcinoma; Cell Line; Cells; Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism; Cultured; Enzyme Inhibitors/pharmacology; Genetic/drug effects/*physiology; Hepatocellular/*metabolism/pathology; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/drug effects/*metabolism/pathology; Humans; Hydroxamic Acids/pharmacology; Liver Neoplasms/*metabolism/pathology; Messenger/metabolism; RNA; Signal Transduction/physiology; Smad3 Protein/metabolism; Transcription; Transforming Growth Factor beta1/*metabolism; Tumor
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chiang John Y L
Description
An account of the resource
BACKGROUND & AIMS: Inhibition of cholesterol 7alpha-hydroxylase (CYP7A1) by bile acids and inflammatory cytokines provides an important mechanism to protect hepatocytes from bile acid toxicity during cholestasis. Transforming growth factor beta1 (TGFbeta1) released by hepatic stellate cells during chronic liver injury plays a critical role in liver inflammation and fibrogenesis. The objective of this study is to investigate the role of TGFbeta1 in hepatic bile acid synthesis. METHODS: mRNA expressions in primary human hepatocytes and HepG2 cells were measured by quantitative real-time polymerase chain reaction. Reporter assay, glutathione-S-transferase pull-down assay, adenovirus-mediated gene transduction, and chromatin immunoprecipitation assay were used to study the mechanism of TGFbeta1 regulation of CYP7A1 gene transcription. RESULTS: TGFbeta1 inhibited the mRNA expression of CYP7A1 and bile acid synthesis in HepG2 cells and primary human hepatocytes. Mothers against decapentaplegic homolog (Smad3) inhibited both CYP7A1 promoter activity and mRNA expression by inhibiting
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">10.1053/j.gastro.2007.08.042</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2007
Bile Acids and Salts/metabolism
Carcinoma
Cell Line
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism
Cultured
Department of Integrative Medical Sciences
Enzyme Inhibitors/pharmacology
Gastroenterology
Genetic/drug effects/*physiology
Hepatocellular/*metabolism/pathology
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/drug effects/*metabolism/pathology
Humans
Hydroxamic Acids/pharmacology
Li Tiangang
Liver Neoplasms/*metabolism/pathology
Messenger/metabolism
NEOMED College of Medicine
RNA
Signal Transduction/physiology
Smad3 Protein/metabolism
Transcription
Transforming Growth Factor beta1/*metabolism
Tumor