| Literature DB >> 20561910 |
Di Shao1, Yang Liu, Xiaojun Liu, Liuluan Zhu, Ying Cui, Anfang Cui, Aijun Qiao, Xingxing Kong, Yong Liu, Quan Chen, Nishith Gupta, Fude Fang, Yongsheng Chang.
Abstract
The peroxisome proliferator-activated receptor-gamma (PPAR-gamma) coactivator-1 beta (PGC-1 beta) is a well-established regulator of the beta-oxidation of fatty acids and the oxidative phosphorylation in mitochondria. However, the underlying mechanism of PGC-1 beta action remains elusive. This study reveals that PGC-1 beta is highly induced during myogenic differentiation and knockdown of endogenous PGC-1 beta by siRNA leads to a decrease in the expression of several mitochondria-related genes. In consistence, the over-expression of PGC-1 beta stimulates its target genes such as cytochrome c, ATP synthase beta and ALAS-1 by its interaction with two transcriptional factors, NRF-1 and ERR alpha. The deletion or mutation of NRF-1 and/or ERR alpha binding sites in target gene promoters attenuates their activation by PGC-1 beta. Moreover, inhibition of NRF-1 or ERR alpha by siRNA ablated the aforesaid function of PGC-1 beta and compromised the oxidative phosphorylation and mitochondrial biogenesis. Taken together, these results confirm the direct interaction of NRF-1 and ERR alpha with PGC-1 beta, and their participation in mitochondrial biogenesis and respiration. (c) 2010 Mitochondria Research Society. Published by Elsevier B.V. All rights reserved.Entities:
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Year: 2010 PMID： 20561910 DOI： 10.1016/j.mito.2010.05.012
Source DB: PubMed Journal: Mitochondrion ISSN： 1567-7249 Impact factor: 4.160