Dexras1 mediates glucocorticoid-associated adipogenesis and diet-induced obesity

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dc.contributor.authorCha, Jiyoung Y.ko
dc.contributor.authorKim, Hyo Jungko
dc.contributor.authorYu, Jung Hwanko
dc.contributor.authorXu, Jingko
dc.contributor.authorKim, Dahamko
dc.contributor.authorPaul, Bindu D.ko
dc.contributor.authorChoi, Hyeonjinko
dc.contributor.authorKim, Seyunko
dc.contributor.authorLee, Yoo Jeongko
dc.contributor.authorHo, Gary P.ko
dc.contributor.authorRao, Fengko
dc.contributor.authorSnyder, Solomon H.ko
dc.contributor.authorKim, Jae-wooko
dc.date.accessioned2014-08-27T02:25:01Z-
dc.date.available2014-08-27T02:25:01Z-
dc.date.created2014-01-13-
dc.date.created2014-01-13-
dc.date.created2014-01-13-
dc.date.created2014-01-13-
dc.date.issued2013-12-
dc.identifier.citationPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.110, no.51, pp.20575 - 20580-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10203/187350-
dc.description.abstractAdipogenesis, the conversion of precursor cells into adipocytes, is associated with obesity and is mediated by glucocorticoids acting via hitherto poorly characterized mechanisms. Dexras1 is a small G protein of the Ras family discovered on the basis of its marked induction by the synthetic glucocorticoid dexamethasone. We show that Dexras1 mediates adipogenesis and diet-induced obesity. Adipogenic differentiation of 3T3-L1 cells is abolished with Dexras1 depletion, whereas overexpression of Dexras1 elicits adipogenesis. Adipogenesis is markedly reduced in mouse embryonic fibroblasts from Dexras1-deleted mice, whereas adiposity and diet-induced weight gain are diminished in the mutant mice.-
dc.languageEnglish-
dc.publisherNATL ACAD SCIENCES-
dc.titleDexras1 mediates glucocorticoid-associated adipogenesis and diet-induced obesity-
dc.typeArticle-
dc.identifier.wosid000328548600056-
dc.identifier.scopusid2-s2.0-84890814669-
dc.type.rimsART-
dc.citation.volume110-
dc.citation.issue51-
dc.citation.beginningpage20575-
dc.citation.endingpage20580-
dc.citation.publicationnamePROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-
dc.identifier.doi10.1073/pnas.1320454110-
dc.contributor.localauthorKim, Seyun-
dc.contributor.nonIdAuthorCha, Jiyoung Y.-
dc.contributor.nonIdAuthorKim, Hyo Jung-
dc.contributor.nonIdAuthorYu, Jung Hwan-
dc.contributor.nonIdAuthorXu, Jing-
dc.contributor.nonIdAuthorKim, Daham-
dc.contributor.nonIdAuthorPaul, Bindu D.-
dc.contributor.nonIdAuthorChoi, Hyeonjin-
dc.contributor.nonIdAuthorLee, Yoo Jeong-
dc.contributor.nonIdAuthorHo, Gary P.-
dc.contributor.nonIdAuthorRao, Feng-
dc.contributor.nonIdAuthorSnyder, Solomon H.-
dc.contributor.nonIdAuthorKim, Jae-woo-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorinsulin-
dc.subject.keywordAuthorcyclic AMP-
dc.subject.keywordAuthornitric oxide-
dc.subject.keywordAuthorCushing disease-
dc.subject.keywordPlusADIPOCYTE DIFFERENTIATION-
dc.subject.keywordPlusCIRCADIAN CLOCK-
dc.subject.keywordPlusMETABOLISM-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusCELL-
dc.subject.keywordPlusPROMOTES-
dc.subject.keywordPlusGTPASE-
dc.subject.keywordPlusGENE-
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