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Article: Negative regulation of adiponectin receptor 1 promoter by insulin via a repressive nuclear inhibitory protein element

TitleNegative regulation of adiponectin receptor 1 promoter by insulin via a repressive nuclear inhibitory protein element
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2008
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet
Citation
FEBS Letters, 2008, v. 582 n. 23-24, p. 3401-3407 How to Cite?
AbstractAdiponectin is an adipose-derived hormone that has anti-diabetic and anti-atherogenic effects through interaction with adiponectin receptors AdipoR1 and AdipoR2. We analyzed the transcriptional regulation of AdipoR1 by insulin. Insulin repressed the promoter activity of AdipoR1 in C2C12 myoblasts via PI3K and Foxo1. Deletion studies demonstrated the presence of a putative insulin-responsive region which is composed of a nuclear inhibitory protein (NIP) binding element. Mutation of the NIP element abrogated the negative regulation of AdipoR1 promoter by insulin. Insulin treatment could induce formation of a protein complex that bound the NIP element. Collectively, our data suggest that a repressive NIP element is involved in the negative regulation of AdipoR1 promoter by insulin. © 2008 Federation of European Biochemical Societies.
Persistent Identifierhttp://hdl.handle.net/10722/92095
ISSN
2015 Impact Factor: 3.519
2015 SCImago Journal Rankings: 2.026
ISI Accession Number ID
Funding AgencyGrant Number
Chinese Academy of Sciences (One Hundred Talents Program and the Knowledge Innovation Program)KSCX1-YW-02
National Natural Science Foundation of China30588002
30470870
Ministry of Science and Technology of China2007CB947100
Funding Information:

We wish to thank Dr. K. L. Guan and Dr. Eric D. Tang from Institute of Gerontology, University of Michigan Medical School Ann Arbor, USA, for providing the plasmids. This work was supported by research grants from Chinese Academy of Sciences (One Hundred Talents Program and the Knowledge Innovation Program KSCX1-YW-02), National Natural Science Foundation of China (30588002 and 30470870), and the Ministry of Science and Technology of China (2007CB947100 and 2007CB947100) to Y. C.

References

 

DC FieldValueLanguage
dc.contributor.authorSun, Xen_HK
dc.contributor.authorHe, Jen_HK
dc.contributor.authorMao, Cen_HK
dc.contributor.authorHan, Ren_HK
dc.contributor.authorWang, Zen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorChen, Yen_HK
dc.date.accessioned2010-09-17T10:35:56Z-
dc.date.available2010-09-17T10:35:56Z-
dc.date.issued2008en_HK
dc.identifier.citationFEBS Letters, 2008, v. 582 n. 23-24, p. 3401-3407en_HK
dc.identifier.issn0014-5793en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92095-
dc.description.abstractAdiponectin is an adipose-derived hormone that has anti-diabetic and anti-atherogenic effects through interaction with adiponectin receptors AdipoR1 and AdipoR2. We analyzed the transcriptional regulation of AdipoR1 by insulin. Insulin repressed the promoter activity of AdipoR1 in C2C12 myoblasts via PI3K and Foxo1. Deletion studies demonstrated the presence of a putative insulin-responsive region which is composed of a nuclear inhibitory protein (NIP) binding element. Mutation of the NIP element abrogated the negative regulation of AdipoR1 promoter by insulin. Insulin treatment could induce formation of a protein complex that bound the NIP element. Collectively, our data suggest that a repressive NIP element is involved in the negative regulation of AdipoR1 promoter by insulin. © 2008 Federation of European Biochemical Societies.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febsleten_HK
dc.relation.ispartofFEBS Lettersen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleNegative regulation of adiponectin receptor 1 promoter by insulin via a repressive nuclear inhibitory protein elementen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.febslet.2008.08.037en_HK
dc.identifier.pmid18789331-
dc.identifier.scopuseid_2-s2.0-53249128847en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-53249128847&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume582en_HK
dc.identifier.issue23-24en_HK
dc.identifier.spage3401en_HK
dc.identifier.epage3407en_HK
dc.identifier.isiWOS:000260806700026-

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