1
40
6
-
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.M110.134890" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M110.134890</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
32182-32191
Issue
42
Volume
285
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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
Ampk-dependent Repression Of Hepatic Gluconeogenesis Via Disruption Of Creb Center Dot Crtc2 Complex By Orphan Nuclear Receptor Small Heterodimer Partner
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-10
Subject
The topic of the resource
activated protein-kinase; binding-protein; Biochemistry & Molecular Biology; creb coactivator crtc2; gene-expression; insulin; metformin; phosphorylation; shp; torc2; transcriptional activity
Creator
An entity primarily responsible for making the resource
Lee J M; Seo W Y; Song K H; Chanda D; Kim Y D; Kim D K; Lee M W; Ryu D; Kim Y H; Noh J R; Lee C H; Chiang J Y L; Koo S H; Choi H S
Description
An account of the resource
Orphan nuclear receptor small heterodimer partner (SHP) plays a key role in transcriptional repression of gluconeogenic enzyme gene expression. Here, we show that SHP inhibited protein kinase A-mediated transcriptional activity of cAMP-response element-binding protein (CREB), a major regulator of glucose metabolism, to modulate hepatic gluconeogenic gene expression. Deletion analysis of phosphoenolpyruvate carboxykinase (PEPCK) promoter demonstrated that SHP inhibited forskolin-mediated induction of PEPCK gene transcription via inhibition of CREB transcriptional activity. In vivo imaging demonstrated that SHP inhibited CREB-regulated transcription coactivator 2 (CRTC2)-mediated cAMP-response element-driven promoter activity. Furthermore, overexpression of SHP using adenovirus SHP decreased CRTC2-dependent elevations in blood glucose levels and PEPCK or glucose-6-phosphatase (G6Pase) expression in mice. SHP and CREB physically interacted and were co-localized in vivo. Importantly, SHP inhibited both wild type CRTC2 and S171A (constitutively active form of CRTC2) coactivator activity and disrupted CRTC2 recruitment on the PEPCK gene promoter. In addition, metformin or overexpression of a constitutively active form of AMPK (Ad-CA-AMPK) inhibited S171A-mediated PEPCK and G6Pase gene expression, and hepatic glucose production and knockdown of SHP partially relieved the metformin- and Ad-CA-AMPK-mediated repression of hepatic gluconeogenic enzyme gene expression in primary rat hepatocytes. In conclusion, our results suggest that a delayed effect of metformin-mediated induction of SHP gene expression inhibits CREB-dependent hepatic gluconeogenesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M110.134890" target="_blank" rel="noreferrer noopener">10.1074/jbc.M110.134890</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
activated protein-kinase
binding-protein
Biochemistry & Molecular Biology
Chanda D
Chiang J Y L
Choi H S
creb coactivator crtc2
gene-expression
insulin
Journal Article or Conference Abstract Publication
Journal of Biological Chemistry
Kim D K
Kim Y D
Kim Y H
Koo S H
Lee C H
Lee J M
Lee M W
metformin
Noh J R
Phosphorylation
Ryu D
Seo W Y
SHP
Song K H
torc2
transcriptional activity
-
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.M111.224352" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M111.224352</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
27971-27979
Issue
32
Volume
286
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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
Cannabinoid Receptor Type 1 (CB1R) Signaling Regulates Hepatic Gluconeogenesis via Induction of Endoplasmic Reticulum-bound Transcription Factor cAMP-responsive Element-binding Protein H (CREBH) in Primary Hepatocytes
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
mice; obesity; Biochemistry & Molecular Biology; risk-factors; er stress; activation; food-intake; dysregulation; endocannabinoid system; overweight patients; rimonabant
Creator
An entity primarily responsible for making the resource
Chanda D; Kim D K; Li T G; Kim Y H; Koo S H; Lee C H; Chiang J Y L; Choi H S
Description
An account of the resource
Activated cannabinoid 1 receptor (CB1R) signaling has been implicated in the development of phenotypes associated with fatty liver, insulin resistance, and impaired suppression of hepatic glucose output. Endoplasmic reticulum stress-associated liver-specific transcription factor CREBH is emerging as a critical player in various hepatic metabolic pathways and regulates hepatic gluconeogenesis in diet-induced obese settings. In this study, we elucidated the critical role of CREBH in mediating CB1R signaling to regulate glucose homeostasis in primary rat and human hepatocytes. mRNA and protein levels and glucose production were analyzed in primary rat and human hepatocytes. ChIP assays were performed together with various transcriptional analyses using standard techniques. CB1R activation by 2-arachidonoylglycerol (2-AG) specifically induced CREBH gene expression via phosphorylation of the JNK signaling pathway and c-Jun binding to the AP-1 binding site in the CREBH gene promoter. 2-AG treatment significantly induced hepatic gluconeogenic gene expression and glucose production in primary hepatocytes, and we demonstrated that the CREBH binding site mutant significantly attenuated 2-AG-mediated activation of the gluconeogenic gene promoter. Endogenous knockdown of CREBH led to ablation of 2-AG-induced gluconeogenic gene expression and glucose production, and the CB1R antagonist AM251 or insulin exhibited repression of CREBH gene induction and subsequently inhibited gluconeogenesis in both rat and human primary hepatocytes. These results demonstrate a novel mechanism of action of activated CB1R signaling to induce hepatic gluconeogenesis via direct activation of CREBH, thereby contributing to a better understanding of the endocannabinoid signaling mechanism involved in regulating the hepatic glucose metabolism.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M111.224352" target="_blank" rel="noreferrer noopener">10.1074/jbc.M111.224352</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
activation
Biochemistry & Molecular Biology
Chanda D
Chiang J Y L
Choi H S
dysregulation
endocannabinoid system
er stress
food-intake
Journal Article or Conference Abstract Publication
Journal of Biological Chemistry
Kim D K
Kim Y H
Koo S H
Lee C H
Li T G
Mice
Obesity
overweight patients
rimonabant
risk-factors
-
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.M111.274514" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M111.274514</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
41972-41984
Issue
49
Volume
286
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Dublin Core
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Title
A name given to the resource
Curcumin Differentially Regulates Endoplasmic Reticulum Stress through Transcriptional Corepressor SMILE (Small Heterodimer Partner-interacting Leucine Zipper Protein)-mediated Inhibition of CREBH (cAMP Responsive Element-binding Protein H)
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-12
Subject
The topic of the resource
phosphorylation; cells; Biochemistry & Molecular Biology; gene-expression; er stress; kinase; atf6; creb/atf-family; hepatic gluconeogenesis; lkb1; zhangfei
Creator
An entity primarily responsible for making the resource
Misra J; Chanda D; Kim D K; Li T G; Koo S H; Back S H; Chiang J Y L; Choi H S
Description
An account of the resource
Curcumin (diferuloylmethane), a major active component of turmeric (Curcuma longa), is a natural polyphenolic compound. Herein the effect of curcumin on endoplasmic reticulum (ER) stress responsive gene expression was investigated. We report that curcumin induces transcriptional corepressor small heterodimer partner-interacting leucine zipper protein (SMILE) gene expression through liver kinase B1 (LKB1)/adenosine monophosphate-activated kinase (AMPK) signaling pathway and represses ER stress-responsive gene transcription in an ER-bound transcription factor specific manner. cAMP responsive element-binding protein H (CREBH) and activating transcription factor 6 (ATF6) are both ER-bound bZIP family transcription factors that are activated upon ER stress. Of interest, we observed that both curcumin treatment and SMILE overexpression only represses CREBH-mediated transactivation of the target gene but not ATF6-mediated transactivation. Knockdown of endogenous SMILE significantly releases the inhibitory effect of curcumin on CREBH transactivation. Intrinsic repressive activity of SMILE is observed in the Gal4 fusion system, and the intrinsic repressive domain is mapped to the C terminus of SMILE spanning amino acid residues 203-269, corresponding to the basic region leucine zipper (bZIP) domain. In vivo interaction assay revealed that through its bZIP domain, SMILE interacts with CREBH and inhibits its transcriptional activity. Interestingly, we observed that SMILE does not interact with ATF6. Furthermore, competition between SMILE and the coactivator peroxisome proliferator-activated receptor alpha (PGC1 alpha) on CREBH transactivation has been demonstrated in vitro and in vivo. Finally, chromatin immunoprecipitation assays revealed that curcumin decreases the binding of PGC-1 alpha and CREBH on target gene promoter in a SMILE-dependent manner. Overall, for the first time we suggest a novel phenomenon that the curcumin/LKB1/AMPK/SMILE/PGC1 alpha pathway differentially regulates ER stress-mediated gene transcription.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M111.274514" target="_blank" rel="noreferrer noopener">10.1074/jbc.M111.274514</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
atf6
Back S H
Biochemistry & Molecular Biology
Cells
Chanda D
Chiang J Y L
Choi H S
creb/atf-family
er stress
gene-expression
hepatic gluconeogenesis
Journal Article or Conference Abstract Publication
Journal of Biological Chemistry
Kim D K
Kinase
Koo S H
Li T G
lkb1
Misra J
Phosphorylation
zhangfei
-
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/hep.23049" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.23049</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
880-892
Issue
3
Volume
50
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
Fenofibrate Differentially Regulates Plasminogen Activator Inhibitor-1 Gene Expression via Adenosine Monophosphate-Activated Protein Kinase-Dependent Induction of Orphan Nuclear Receptor Small Heterodimer Partner
Publisher
An entity responsible for making the resource available
Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-09
Subject
The topic of the resource
cells; binding; complex; fibrosis; Gastroenterology & Hepatology; promoter; beta; mechanisms; pai-1; shp; smad3
Creator
An entity primarily responsible for making the resource
Chanda D; Lee C H; Kim Y H; Noh J R; Kim D K; Park J H; Hwang J H; Lee M R; Jeong K H; Lee I K; Kweon G R; Shong M; Oh G T; Chiang J Y L; Choi H S
Description
An account of the resource
Plasminogen activator inhibitor type I (PAI-1) is a marker of the fibrinolytic system and serves as a possible predictor for hepatic metabolic syndromes. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR alpha) agonist, is a drug used for treatment of hyperlipidemia. Orphan nuclear receptor small heterodimer partner (SHP) plays a key role in transcriptional repression of crucial genes involved in various metabolic pathways. In this Study, we show that fenofibrate increased SHP gene expression in cultured liver cells and in the normal and diabetic mouse liver by activating the adenosine monophosphate-activated protein kinase (AMPK signaling pathway in a PPAR alpha-independent manner. Administration of transforming growth factor beta (TGF-beta) or a methionine-deficient and choline-deficient (MCD) diet to induce the progressive fibrosing steatohepatitis model in C57BL/6 mice was significantly reversed by fenofibrate via AMPK-mediated induction of SHP gene expression with a dramatic decrease in PAI-1 messenger RNA (mRNA) and protein expression along with other fibrotic marker genes. No reversal was observed in SHP null mice treated with fenofibrate. Treatment with another PPAR alpha agonist, WY14643, showed contrasting effects on these marker gene expressions in wild-type and SHP null mice, demonstrating the specificity of fenofibrate in activating AMPK signaling. Fenofibrate exhibited a differential inhibitory pattern on PAI-1 gene expression depending on the transcription factors inhibited by SHP. Conclusion: By demonstrating that a PPAR alpha-independent fenofibrate-AMPK-SHP regulatory cascade can play a key role in PAI-1 gene down-regulation and reversal of fibrosis, our study suggests that various AMPK activators regulating SHP might provide a novel pharmacologic option in ameliorating hepatic metabolic syndromes. (HEPATOLOGY 2009;50:880-892.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.23049" target="_blank" rel="noreferrer noopener">10.1002/hep.23049</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
beta
Binding
Cells
Chanda D
Chiang J Y L
Choi H S
complex
Fibrosis
Gastroenterology & Hepatology
Hepatology
Hwang J H
Jeong K H
Journal Article or Conference Abstract Publication
Kim D K
Kim Y H
Kweon G R
Lee C H
Lee I K
Lee M R
mechanisms
Noh J R
Oh G T
PAI-1
Park J H
promoter
Shong M
SHP
smad3
-
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.0068845" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0068845</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
11-11
Issue
7
Volume
8
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
Hepatic Cannabinoid Receptor Type 1 Mediates Alcohol-Induced Regulation of Bile Acid Enzyme Genes Expression Via CREBH
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
2013
2013-07
Subject
The topic of the resource
metabolism; Ohio; mice; Signaling; Signal transduction; liver; Homeostasis; transcription factor; Genes; exposure; Acids; er stress; endoplasmic-reticulum stress; Science & Technology - Other Topics; insulin-resistance; cholesterol 7-alpha-hydroxylase; human hepatocytes; Rodents; Bile acids; alcohol; element-binding protein; gene-expression; endocannabinoid system; bound; cb1 receptors; leptin resistance; Liver diseases; Diabetes mellitus; insulin-resistance; insulin; Fatty liver; hepatocytes; Sciences: Comprehensive Works; Alcohols; Bile; activation; Damage prevention; Deregulation; Muridae; Regulatory mechanisms (biology); RNA extraction; Synthesis
Creator
An entity primarily responsible for making the resource
Chanda D; Kim Y H; Li T; Misra J; Kim D K; Kim J R; Kwon J; Jeong W I; Ahn S H; Park T S; Koo S H; Chiang J Y L; Lee C H; Choi H S
Description
An account of the resource
Bile acids concentration in liver is tightly regulated to prevent cell damage. Previous studies have demonstrated that deregulation of bile acid homeostasis can lead to cholestatic liver disease. Recently, we have shown that ER-bound transcription factor Crebh is a downstream effector of hepatic Cb1r signaling pathway. In this study, we have investigated the effect of alcohol exposure on hepatic bile acid homeostasis and elucidated the mediatory roles of Cb1r and Crebh in this process. We found that alcohol exposure or Cb1r-agonist 2-AG treatment increases hepatic bile acid synthesis and serum ALT, AST levels in vivo alongwith significant increase in Crebh gene expression and activation. Alcohol exposure activated Cb1r, Crebh, and perturbed bile acid homeostasis. Overexpression of Crebh increased the expression of key bile acid synthesis enzyme genes via direct binding of Crebh to their promoters, whereas Cb1r knockout and Crebh-knockdown mice were protected against alcohol-induced perturbation of bile acid homeostasis. Interestingly, insulin treatment protected against Cb1r-mediated Crebh-induced disruption of bile acid homeostasis. Furthermore, Crebh expression and activation was found to be markedly increased in insulin resistance conditions and Crebh knockdown in diabetic mice model (db/db) significantly reversed alcohol-induced disruption of bile acid homeostasis. Overall, our study demonstrates a novel regulatory mechanism of hepatic bile acid metabolism by alcohol via Cb1r-mediated activation of Crebh, and suggests that targeting Crebh can be of therapeutic potential in ameliorating alcohol-induced perturbation of bile acid homeostasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0068845" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0068845</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
Acids
activation
Ahn S H
Alcohol
Alcohols
Bile
BILE acids
bound
cb1 receptors
Chanda D
Chiang J Y L
Choi H S
cholesterol 7-alpha-hydroxylase
Damage prevention
Deregulation
Diabetes Mellitus
element-binding protein
endocannabinoid system
endoplasmic-reticulum stress
er stress
exposure
Fatty Liver
gene-expression
Genes
hepatocytes
Homeostasis
human hepatocytes
insulin
insulin-resistance
Jeong W I
Journal Article or Conference Abstract Publication
Kim D K
Kim J R
Kim Y H
Koo S H
Kwon J
Lee C H
leptin resistance
Li T
Liver
Liver Diseases
Metabolism
Mice
Misra J
Muridae
Ohio
Park T S
PloS one
Regulatory mechanisms (biology)
RNA extraction
Rodents
Science & Technology - Other Topics
Sciences: Comprehensive Works
Signal Transduction
Signaling
Synthesis
transcription factor
-
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.M112.339887" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M112.339887</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
37098-37108
Issue
44
Volume
287
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
Orphan Nuclear Receptor Small Heterodimer Partner Negatively Regulates Growth Hormone-mediated Induction Of Hepatic Gluconeogenesis Through Inhibition Of Signal Transducer And Activator Of Transcription 5 (stat5) Transactivation
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-10
Subject
The topic of the resource
ampk; ataxia-telangiectasia; atm; Biochemistry & Molecular Biology; expression; Glucose; glucose-6-phosphatase gene; involvement; metformin; protein kinase; shp
Creator
An entity primarily responsible for making the resource
Kim Y D; Li T G; Ahn S W; Kim D K; Lee J M; Hwang S L; Kim Y H; Lee C H; Lee I K; Chiang J Y L; Choi H S
Description
An account of the resource
Growth hormone (GH) is a key metabolic regulator mediating glucose and lipid metabolism. Ataxia telangiectasia mutated (ATM) is a member of the phosphatidylinositol 3-kinase superfamily and regulates cell cycle progression. The orphan nuclear receptor small heterodimer partner (SHP: NR0B2) plays a pivotal role in regulating metabolic processes. Here, we studied the role of ATM on GH-dependent regulation of hepatic gluconeogenesis in the liver. GH induced phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase gene expression in primary hepatocytes. GH treatment and adenovirus-mediated STAT5 overexpression in hepatocytes increased glucose production, which was blocked by a JAK2 inhibitor, AG490, dominant negative STAT5, and STAT5 knockdown. We identified a STAT5 binding site on the PEPCK gene promoter using reporter assays and point mutation analysis. Up-regulation of SHP by metformin-mediated activation of the ATM-AMP-activated protein kinase pathway led to inhibition of GH-mediated induction of hepatic gluconeogenesis, which was abolished by an ATM inhibitor, KU-55933. Immunoprecipitation studies showed that SHP physically interacted with STAT5 and inhibited STAT5 recruitment on the PEPCK gene promoter. GH-induced hepatic gluconeogenesis was decreased by either metformin or Ad-SHP, whereas the inhibition by metformin was abolished by SHP knockdown. Finally, the increase of hepatic gluconeogenesis following GH treatment was significantly higher in the liver of SHP null mice compared with that of wildtype mice. Overall, our results suggest that the ATM-AMP-activated protein kinase-SHP network, as a novel mechanism for regulating hepatic glucose homeostasis via a GH-dependent pathway, may be a potential therapeutic target for insulin resistance.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M112.339887" target="_blank" rel="noreferrer noopener">10.1074/jbc.M112.339887</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Ahn S W
AMPK
ataxia-telangiectasia
atm
Biochemistry & Molecular Biology
Chiang J Y L
Choi H S
expression
GLUCOSE
glucose-6-phosphatase gene
Hwang S L
involvement
Journal Article or Conference Abstract Publication
Journal of Biological Chemistry
Kim D K
Kim Y D
Kim Y H
Lee C H
Lee I K
Lee J M
Li T G
metformin
protein kinase
SHP