P32 REGULATES MITOCHONDRIAL MORPHOLOGY AND DYNAMICS THROUGH PARKIN

P32 REGULATES MITOCHONDRIAL MORPHOLOGY AND DYNAMICS THROUGH PARKIN
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DOI:
10.1016/j.neuroscience.2011.10.003
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发表时间:
2011-12-29
期刊:
影响因子:
3.3
通讯作者:
Chung, K. K. K.
Chung, K. K. K.
中科院分区:
医学3区
文献类型:
--
作者:
Li, Y.;Wan, O. W.;Chung, K. K. K.

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帕金突变首先在一组日本患者中发现,这些患者患有常染色体隐性遗传的青少年帕金森综合征,临床症状与特发性帕金森病(PD)相似。Parkin是一种E3连接酶,靶向许多底物进行泛素化。最近的研究表明,parkin与另一种家族连锁的PD基因产物PINK1一起参与细胞中线粒体动力学的调节。在这项研究中,我们已经确定了线粒体蛋白p32作为一种新的帕金在大脑中的相互作用。我们发现p32可以通过自噬促进parkin降解来调节线粒体的形态和动力学。这些结果表明,parkin可能是一个重要的效应器在调节线粒体的形态和动力学。(C)2011年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Mutations in parkin were first identified in a group of Japanese patients who developed autosomal recessive juvenile Parkinsonism with clinical symptoms similar to idiopathic Parkinson's disease (PD). Parkin is an E3 ligase that targets a number of substrates for ubiquitination. Recent studies show that parkin together with PINK1, another familial-linked PD gene product, is involved in the regulation of mitochondrial dynamics in the cell. In this study, we have identified a mitochondrial protein p32 as a novel interactor of parkin in the brain. We found that p32 can regulate mitochondrial morphology and dynamics by promoting parkin degradation through autophagy. These results suggest that parkin might be an important effector in the regulation of morphology and dynamics of mitochondria. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.