Parkin enhances mitochondrial biogenesis in proliferating cells
Parkin enhances mitochondrial biogenesis in proliferating cells
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DOI：
10.1093/hmg/ddl006
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发表时间：
2006-03-15
影响因子：
3.5
通讯作者：
Matsumoto, T
中科院分区：
文献类型：
--
作者：
Kuroda, Y;Mitsui, T;Matsumoto, T
我们描述了Parkin的一个新功能，它是一种环蛋白，它精心参与了线粒体的生物发生。Parkin位于增殖细胞的线粒体细胞器内。抗增殖治疗将parkin从线粒体释放到细胞质。药理处理结果表明，当通透性转换孔打开时，parkin从线粒体释放出来。在分化的细胞中也观察到线粒体外的定位。在增殖细胞中，parkin过表达可促进线粒体DNA的转录和复制，而siRNA抑制parkin可抑制线粒体DNA的转录和复制。Parkin与线粒体转录因子A(TFAM)相关，增强TFAM介导的线粒体转录。这些结果表明，在增殖细胞中，Parkin参与了线粒体转录/复制的调控，而不是泛素介导的蛋白质降解系统。
We describe a novel function of parkin, a RING protein, which is elaborately involved in mitochondrial biogenesis. Parkin was located within the mitochondrial organelle of proliferating cells. Anti-proliferative treatments released parkin from mitochondria to cytosol. Results of pharmacological treatments indicate that parkin was released from mitochondria when permeability transition pore was opened. The extra-mitochondrial localization was also observed in differentiated cells. In proliferating cells, transcription and replication of mitochondrial DNA was enhanced by parkin overexpression and attenuated by parkin suppression with siRNA. Parkin was associated with mitochondrial transcription factor A (TFAM) and enhanced TFAM-mediated mitochondrial transcription. These results indicate that parkin is involved in the regulation of mitochondrial transcription/replication other than the ubiquitin-mediated protein degradation system in proliferating cells.