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基因程序特异性调节 PGC-1{alpha} 活性。

Gene program-specific regulation of PGC-1{alpha} activity.

机构信息

Department of Biochemistry and Molecular Biology, University of Southern Denmark.

出版信息

Genes Dev. 2011 Jul 15;25(14):1453-8. doi: 10.1101/gad.2076411.

DOI:10.1101/gad.2076411
PMID:21764849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3143934/
Abstract

Peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1 α (PGC-1α) activation coordinates induction of the hepatic fasting response through coactivation of numerous transcription factors and gene programs. In the June 15, 2011, issue of Genes & Development, Lustig and colleagues (pp. 1232-1244) demonstrated that phosphorylation of PGC-1α by the p70 ribosomal protein S6 kinase 1 (S6K1) specifically interfered with the interaction between PGC-1α and HNF4α in liver and blocked the coactivation of the gluconeogenic target genes. This demonstrates how independent fine-tuning of gene programs coregulated by the same coactivator can be obtained.

摘要

过氧化物酶体增殖物激活受体 γ(PPARγ)共激活因子 1α(PGC-1α)的激活通过共激活许多转录因子和基因程序来协调肝脏禁食反应的诱导。在 2011 年 6 月 15 日的《基因与发育》杂志上,Lustig 及其同事(第 1232-1244 页)表明,p70 核糖体蛋白 S6 激酶 1(S6K1)对 PGC-1α 的磷酸化特异性地干扰了 PGC-1α与肝 HNF4α 之间的相互作用,并阻止了糖异生靶基因的共激活。这证明了如何通过相同的共激活因子来获得对受共同调节的基因程序的独立微调。

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本文引用的文献

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Separation of the gluconeogenic and mitochondrial functions of PGC-1{alpha} through S6 kinase.通过 S6 激酶将 PGC-1α 的糖异生和线粒体功能分离。
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The genetic ablation of SRC-3 protects against obesity and improves insulin sensitivity by reducing the acetylation of PGC-1{alpha}.SRC-3的基因消融通过减少PGC-1α的乙酰化来预防肥胖并改善胰岛素敏感性。
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