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

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dc.contributor.authorKim, Hye Youngko
dc.contributor.authorCho, Hyun Kookko
dc.contributor.authorYoo, Seong Keunko
dc.contributor.authorCheong, JaeHunko
dc.date.accessioned2013-03-13T03:27:28Z-
dc.date.available2013-03-13T03:27:28Z-
dc.date.created2012-12-10-
dc.date.created2012-12-10-
dc.date.issued2012-10-
dc.identifier.citationEXPERIMENTAL AND MOLECULAR MEDICINE, v.44, no.10, pp.622 - 632-
dc.identifier.issn1226-3613-
dc.identifier.urihttp://hdl.handle.net/10203/104360-
dc.description.abstractSix 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 alpha, IL-1 beta, 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.-
dc.languageEnglish-
dc.publisherKOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY-
dc.subjectADIPOSE-RELATED PROTEIN-
dc.subjectNECROSIS-FACTOR-ALPHA-
dc.subjectTRANSACTIVATION FUNCTION-
dc.subjectPOSITIVE REGULATOR-
dc.subjectINSULIN-RESISTANCE-
dc.subjectINFLAMMATION-
dc.subjectEXPRESSION-
dc.subjectGENE-
dc.subjectADIPOCYTES-
dc.subjectTISSUE-
dc.titleHepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation-
dc.typeArticle-
dc.identifier.wosid000310770700007-
dc.identifier.scopusid2-s2.0-84868121549-
dc.type.rimsART-
dc.citation.volume44-
dc.citation.issue10-
dc.citation.beginningpage622-
dc.citation.endingpage632-
dc.citation.publicationnameEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.identifier.doi10.3858/emm.2012.44.10.071-
dc.contributor.localauthorYoo, Seong Keun-
dc.contributor.nonIdAuthorKim, Hye Young-
dc.contributor.nonIdAuthorCho, Hyun Kook-
dc.contributor.nonIdAuthorCheong, JaeHun-
dc.description.isOpenAccessY-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorfatty liver-
dc.subject.keywordAuthorgluconeogenesis-
dc.subject.keywordAuthorhepatitis B virus X protein-
dc.subject.keywordAuthorinsulin resistance-
dc.subject.keywordAuthorliver-
dc.subject.keywordAuthorSTEAP4 protein-
dc.subject.keywordAuthorhuman-
dc.subject.keywordPlusADIPOSE-RELATED PROTEIN-
dc.subject.keywordPlusNECROSIS-FACTOR-ALPHA-
dc.subject.keywordPlusTRANSACTIVATION FUNCTION-
dc.subject.keywordPlusPOSITIVE REGULATOR-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusADIPOCYTES-
dc.subject.keywordPlusTISSUE-
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