1
40
3
-
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/10.1016/j.freeradbiomed.2009.06.017" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2009.06.017</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
767-778
Issue
6
Volume
47
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Role of peroxisome proliferator-activated receptor-alpha in fasting-mediated oxidative stress
Publisher
An entity responsible for making the resource available
Free Radical Biology and Medicine
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
Aldehyde dehydrogenase; Biochemistry & Molecular Biology; differential expression; dismutase; Endocrinology & Metabolism; Fasting; fatty-acid oxidation; glutathione-s-transferase; hepatic steatosis; Lipid peroxidation; Lipid peroxidation; liver; manganese-superoxide-dismutase; mitochondrial aldehyde dehydrogenase; nitric-oxide; Null mice; oxidative stress; PPAR-alpha; PPAR-alpha; Protein nitration; Protein oxidation; rat-liver; Steatosis; Superoxide
Creator
An entity primarily responsible for making the resource
Abdelmegeed M A; Moon K H; Hardwick J P; Gonzalez F J; Song B J
Description
An account of the resource
The peroxisome proliferator-activated receptor-alpha (PPAR alpha) regulates lipid homeostasis, particularly in the liver. This study was aimed at elucidating the relationship between hepatosteatosis and oxidative stress during fasting. Fasted Ppara-null mice exhibited marked hepatosteatosis, which was associated with elevated levels of lipid peroxidation, nitric oxide synthase activity, and hydrogen peroxide accumulation. Total glutathione (GSH), mitochondrial GSH, and the activities of major antioxidant enzymes were also lower in the fasted Ppara-null mice. Consequently, the number and extent of nitrated proteins were markedly increased in the fasted Ppara-null mice, although high levels of protein nitration were still detected in the fed Ppara-null mice while many oxidatively modified proteins were only found in the fasted Ppara-null mice. However, the role of inflammation in increased oxidative stress in the fasted Ppara-null mice was minimal based on the similar levels of tumor necrosis factor-alpha change in all groups. These results with increased oxidative stress observed in the fasted Ppara-null mice compared with other groups demonstrate a role for PPAR alpha in fasting-mediated oxidative stress and that inhibition of PPAR alpha functions may increase the susceptibility to oxidative damage in the presence of another toxic agent. Published by Elsevier Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2009.06.017" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2009.06.017</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
Abdelmegeed M A
Aldehyde Dehydrogenase
Biochemistry & Molecular Biology
differential expression
dismutase
Endocrinology & Metabolism
Fasting
fatty-acid oxidation
Free Radical Biology and Medicine
glutathione-s-transferase
Gonzalez F J
Hardwick J P
hepatic steatosis
Journal Article or Conference Abstract Publication
Lipid Peroxidation
Liver
manganese-superoxide-dismutase
mitochondrial aldehyde dehydrogenase
Moon K H
nitric-oxide
Null mice
Oxidative Stress
PPAR-alpha
Protein nitration
Protein oxidation
rat-liver
Song B J
Steatosis
superoxide
-
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/10.1021/acs.jproteorne.8b00417" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/acs.jproteorne.8b00417</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
3740-3748
Issue
11
Volume
17
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
d2ome, Software for in Vivo Protein Turnover Analysis Using Heavy Water Labeling and LC-MS, Reveals Alterations of Hepatic Proteome Dynamics in a Mouse Model of NAFLD
Publisher
An entity responsible for making the resource available
Journal of Proteome Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-11
Subject
The topic of the resource
40S ribosomal proteins; algorithm; amino-acids; Biochemistry & Molecular Biology; dna; in vivo protein turnover; isotopomer; Mass spectrometry; metabolic labeling; NAFLD; nonlinear least-squares modeling; peak detection and integration; proliferation; protein half-life; proteome dynamics; proteostasis; quantification; rates; respiratory-chain; steatosis; UPR
Creator
An entity primarily responsible for making the resource
Sadygov R G; Avva J; Rahman M; Lee K; Ilchenko S; Kasumov T; Borzou A
Description
An account of the resource
Metabolic labeling with heavy water followed by LC-MS is a high throughput approach to study proteostasis in vivo. Advances in mass spectrometry and sample processing have allowed consistent detection of thousands of proteins at multiple time points. However, freely available automated bioinformatics tools to analyze and extract protein decay rate constants are lacking. Here, we describe d2ome-a robust, automated software solution for in vivo protein turnover analysis. d2ome is highly scalable, uses innovative approaches to nonlinear fitting, implements Grubbs' outlier detection and removal, uses weighted-averaging of replicates, applies a data dependent elution time windowing, and uses mass accuracy in peak detection. Here, we discuss the application of d2ome in a comparative study of protein turnover in the livers of normal vs Western diet-fed LDLR-/- mice (mouse model of nonalcoholic fatty liver disease), which contained 256 LC-MS experiments. The study revealed reduced stability of 40S ribosomal protein subunits in the Western diet-fed mice.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/acs.jproteorne.8b00417" target="_blank" rel="noreferrer noopener">10.1021/acs.jproteorne.8b00417</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2018
40S ribosomal proteins
algorithm
amino-acids
Avva J
Biochemistry & Molecular Biology
Borzou A
Department of Pharmaceutical Sciences
DNA
Ilchenko S
in vivo protein turnover
isotopomer
Journal Article
Journal of proteome research
Kasumov T
Lee K
Mass spectrometry
metabolic labeling
NAFLD
NEOMED College of Pharmacy
nonlinear least-squares modeling
peak detection and integration
proliferation
protein half-life
Proteome dynamics
proteostasis
quantification
Rahman M
rates
respiratory-chain
Sadygov R G
Steatosis
UPR
-
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/10.1016/j.jhep.2018.10.037" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jhep.2018.10.037</a>
Pages
237–248
Issue
2
Volume
70
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
Effect of ethanol on lipid metabolism.
Publisher
An entity responsible for making the resource available
Journal of hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Alcohol-related liver disease; Lipid homeostasis; Metabolism; Steatosis
Creator
An entity primarily responsible for making the resource
You Min; Arteel Gavin E
Description
An account of the resource
Hepatic lipid metabolism is a series of complex processes that control influx and efflux of not only hepatic lipid pools, but also organismal pools. Lipid homeostasis is usually tightly controlled by expression, substrate supply, oxidation and secretion that keep hepatic lipid pools relatively constant. However, perturbations of any of these processes can lead to lipid accumulation in the liver. Although it is thought that these responses are hepatic arms of the 'thrifty genome', they are maladaptive in the context of chronic fatty liver diseases. Ethanol is likely unique among toxins, in that it perturbs almost all aspects of hepatic lipid metabolism. This complex response is due in part to the large metabolic demand placed on the organ by alcohol metabolism, but also appears to involve more nuanced changes in expression and substrate supply. The net effect is that steatosis is a rapid response to alcohol abuse. Although transient steatosis is largely an inert pathology, the chronicity of alcohol-related liver disease seems to require steatosis. Better and more specific understanding of the mechanisms by which alcohol causes steatosis may therefore translate into targeted therapies to treat alcohol-related liver disease and/or prevent its progression.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jhep.2018.10.037" target="_blank" rel="noreferrer noopener">10.1016/j.jhep.2018.10.037</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).
2019
Alcohol-related liver disease
Arteel Gavin E
Department of Pharmaceutical Sciences
Journal of hepatology
Lipid homeostasis
Metabolism
NEOMED College of Pharmacy
Steatosis
You Min