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核受体共抑制因子与过氧化物酶体增殖物激活受体γ

Nuclear receptor corepressors and PPARgamma.

作者信息

Cohen Ronald N

机构信息

Section of Endocrinology, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA.

出版信息

Nucl Recept Signal. 2006;4:e003. doi: 10.1621/nrs.04003. Epub 2006 Feb 8.

DOI:10.1621/nrs.04003
PMID:16604166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1402213/
Abstract

The nuclear receptor corepressors NCoR and SMRT repress gene transcription by recruiting a histone deacetylase complex. Their roles in PPARgamma action have been controversial. Recent evidence, however, suggests that NCoR and SMRT repress PPARgamma-mediated transcriptional activity on specific promoters in the adipocyte. In addition, by repressing PPARgamma action, these corepressors inhibit the ability of adipocyte differentiation to proceed. A further understanding of corepressor action in the adipocyte will provide insight into the balance of forces regulating adipogenesis, insulin sensitivity, and Type 2 diabetes mellitus.

摘要

核受体共抑制因子NCoR和SMRT通过募集组蛋白去乙酰化酶复合体来抑制基因转录。它们在PPARγ作用中的角色一直存在争议。然而,最近的证据表明,NCoR和SMRT在脂肪细胞中抑制PPARγ介导的特定启动子上的转录活性。此外,通过抑制PPARγ的作用,这些共抑制因子抑制脂肪细胞分化的进程。对脂肪细胞中共抑制因子作用的进一步了解将有助于深入了解调节脂肪生成、胰岛素敏感性和2型糖尿病的各种力量的平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b2/1402213/b27abe9e7710/nrs04003.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b2/1402213/b27abe9e7710/nrs04003.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b2/1402213/b27abe9e7710/nrs04003.f1.jpg

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