1
40
2
-
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.livres.2017.08.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.livres.2017.08.001</a>
Pages
96–102
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
Activating transcription factor 3 in immune response and metabolic regulation.
Publisher
An entity responsible for making the resource available
Liver research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-09
Subject
The topic of the resource
Activating transcription factor 3 (ATF3); Glucose homeostasis; Immune; Liver injury; Oncogenesis
Creator
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Jadhav Kavita; Zhang Yanqiao
Description
An account of the resource
Activating transcription factor 3 (ATF3) is a member of the ATF/cAMP-response element binding protein (CREB) family of transcription factors. In response to stress stimuli, ATF3 forms dimers to activate or repress gene expression. Further, ATF3 modulates the immune response, atherogenesis, cell cycle, apoptosis, and glucose homeostasis. Recent studies have shown that ATF3 may also be involved in pathogenesis of other diseases. However, more studies are needed to determine the role of ATF3 in metabolic regulation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.livres.2017.08.001" target="_blank" rel="noreferrer noopener">10.1016/j.livres.2017.08.001</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
Activating transcription factor 3 (ATF3)
Glucose homeostasis
Immune
Jadhav Kavita
Liver injury
Liver research
Oncogenesis
Zhang Yanqiao
-
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.livres.2017.05.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.livres.2017.05.001</a>
Pages
3–9
Issue
1
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
Bile acid metabolism and signaling in liver disease and therapy.
Publisher
An entity responsible for making the resource available
Liver research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-06
Subject
The topic of the resource
Bile acid metabolism; Cholestatic liver; diseases Metabolic diseases
Creator
An entity primarily responsible for making the resource
Chiang John Y L
Description
An account of the resource
Bile acids play a critical role in the regulation of glucose, lipid, and energy metabolism through activation of the nuclear bile acid receptor farnesoid X receptor (FXR) and membrane G protein-coupled bile acid receptor-1 (Gpbar-1, aka TGR5). Agonist activation of FXR and TGR5 improves insulin and glucose sensitivity and stimulates energy metabolism to prevent diabetes, obesity, and non-alcoholic fatty liver disease (NAFLD). Bile acids have both pro- and anti-inflammatory actions through FXR and TGR5 in the intestine and liver. In the intestine, bile acids activate FXR and TGR5 to stimulate stimulate fibroblast growth factor 15 and glucagon-like peptide-1 secretion. FXR and TGR5 agonists may have therapeutic potential for treating liver-related metabolic diseases, such as diabetes and NAFLD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.livres.2017.05.001" target="_blank" rel="noreferrer noopener">10.1016/j.livres.2017.05.001</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
Bile acid metabolism
Chiang John Y L
Cholestatic liver
Department of Integrative Medical Sciences
diseases Metabolic diseases
Liver research
NEOMED College of Medicine