NDLI: Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation.

Please wait, while we are loading the content...

The hydrophobic amino acids involved in the interdomain association of phospholipase D1 regulate the shuttling of phospholipase D1 from vesicular organelles into the nucleus.

Peroxisome proliferator-activated receptor Î´ agonist attenuates hepatic steatosis by anti-inflammatory mechanism.

Protective effects of transduced Tat-DJ-1 protein against oxidative stress and ischemic brain injury

Increased arginase II activity contributes to endothelial dysfunction through endothelial nitric oxide synthase uncoupling in aged mice.

Antiobesity activity of a sphingosine 1-phosphate analogue FTY720 observed in adipocytes and obese mouse model

Effects of echinomycin on endothelin-2 expression and ovulation in immature rats primed with gonadotropins.

Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation.

Year: 2012 Volume: 44 Issue: 9

Year: 2012 Volume: 44 Issue: 8

Year: 2012 Volume: 44 Issue: 7

Year: 2012 Volume: 44 Issue: 6

Year: 2012 Volume: 44 Issue: 5

Year: 2012 Volume: 44 Issue: 4

Year: 2012 Volume: 44 Issue: 3

Year: 2012 Volume: 44 Issue: 2

Year: 2012 Volume: 44 Issue: 1

Year: 2011 Volume: 43

Year: 2010 Volume: 42

Year: 2009 Volume: 41

Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kim, Hye Young Cho, Hyun Kook Yoo, Seong Keun Cheong, Jae Hun
Description	Author Affiliation: Kim HY ( Department of Molecular Biology College of Natural Sciences Pusan National University Busan 609-735, Korea.)
Abstract	Six transmembrane protein of prostate 2 (STAMP2) plays a key role in linking inflammatory and diet-derived signals to systemic metabolism. STAMP2 is induced by nutrients/feeding as well as by cytokines such as TNF , IL-1ß, and IL-6. Here, we demonstrated that STAMP2 protein physically interacts with and decreases the stability of hepatitis B virus X protein (HBx), thereby counteracting HBx-induced hepatic lipid accumulation and insulin resistance. STAMP2 suppressed the HBx-mediated transcription of lipogenic and adipogenic genes. Furthermore, STAMP2 prevented HBx-induced degradation of IRS1 protein, which mediates hepatic insulin signaling, as well as restored insulin-mediated inhibition of gluconeogenic enzyme expression, which are gluconeogenic genes. We also demonstrated reciprocal expression of HBx and STAMP2 in HBx transgenic mice. These results suggest that hepatic STAMP2 antagonizes HBx-mediated hepatocyte dysfunction, thereby protecting hepatocytes from HBV gene expression.
File Format	HTM / HTML
ISSN	12263613
e-ISSN	20926413
DOI	10.3858/emm.2012.44.10.071
Journal	Experimental & Molecular Medicine
Issue Number	10
Volume Number	44
Language	English
Publisher	Macmillan Publishers Limited
Publisher Date	2012-10-31
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology Discipline Biochemistry Lipid Metabolism Liver Metabolism Membrane Proteins Physiology Oxidoreductases Trans-activators Animals Gene Expression Gluconeogenesis Genetics Hep G2 Cells Insulin Pharmacology Insulin Receptor Substrate Proteins Insulin Resistance Physiopathology Mice Mice, Inbred C57bl Mice, Inbred Cba Mice, Transgenic Phosphorylation Protein Binding Protein Processing, Post-translational Proteolysis Receptor, Insulin Transcriptional Activation Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Molecular Biology Clinical Biochemistry Molecular Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Hyperinsulinemia Enhances Hepatic Expression of the Fatty Acid Transporter Cd36 and Provokes Hepatosteatosis and Hepatic Insulin $Resistance^{*}$

Insulin regulates retinol dehydrogenase expression and all-trans-retinoic acid biosynthesis through FoxO1.

Metformin suppresses hepatic gluconeogenesis through induction of SIRT1 and GCN5.

Par14 protein associates with insulin receptor substrate 1 (IRS-1), thereby enhancing insulin-induced IRS-1 phosphorylation and metabolic actions.

Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha)-deficient mice.

Myostatin induces insulin resistance via Casitas B-lineage lymphoma b (Cblb)-mediated degradation of insulin receptor substrate 1 (IRS1) protein in response to high calorie diet intake.

Insulin Regulates Retinol Dehydrogenase Expression and All-trans-retinoic Acid Biosynthesis through FoxO1*

Carrageenan Inhibits Insulin Signaling through GRB10-mediated Decrease in Tyr(P)-IRS1 and through Inflammation-induced Increase in Ser(P)307-IRS1.

Stat5 is a physiological substrate of the insulin receptor.

Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation.

Similar Documents

Hyperinsulinemia Enhances Hepatic Expression of the Fatty Acid Transporter Cd36 and Provokes Hepatosteatosis and Hepatic Insulin $Resistance^{*}$

Insulin regulates retinol dehydrogenase expression and all-trans-retinoic acid biosynthesis through FoxO1.

Metformin suppresses hepatic gluconeogenesis through induction of SIRT1 and GCN5.

Par14 protein associates with insulin receptor substrate 1 (IRS-1), thereby enhancing insulin-induced IRS-1 phosphorylation and metabolic actions.

Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha)-deficient mice.

Myostatin induces insulin resistance via Casitas B-lineage lymphoma b (Cblb)-mediated degradation of insulin receptor substrate 1 (IRS1) protein in response to high calorie diet intake.

Insulin Regulates Retinol Dehydrogenase Expression and All-trans-retinoic Acid Biosynthesis through FoxO1*

Carrageenan Inhibits Insulin Signaling through GRB10-mediated Decrease in Tyr(P)-IRS1 and through Inflammation-induced Increase in Ser(P)307-IRS1.

Stat5 is a physiological substrate of the insulin receptor.

Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation.