清除群体中的病态线粒体。
Culling sick mitochondria from the herd.
机构信息
Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.
出版信息
J Cell Biol. 2010 Dec 27;191(7):1225-7. doi: 10.1083/jcb.201011068.
The PINK1-Parkin pathway plays a critical role in mitochondrial quality control by selectively targeting damaged mitochondria for autophagy. In this issue, Tanaka et al. (2010. J. Cell Biol. doi: 10.1083/jcb.201007013) demonstrate that the AAA-type ATPase p97 acts downstream of PINK1 and Parkin to segregate fusion-incompetent mitochondria for turnover. p97 acts by targeting the mitochondrial fusion-promoting factor mitofusin for degradation through an endoplasmic reticulum-associated degradation (ERAD)-like mechanism.
PINK1-Parkin 通路通过选择性地靶向受损线粒体进行自噬，在维持线粒体质量控制方面发挥着关键作用。在本期杂志中，Tanaka 等人（2010. J. Cell Biol. doi: 10.1083/jcb.201007013）证明，AAA 型 ATP 酶 p97 在 PINK1 和 Parkin 下游发挥作用，将融合无能的线粒体进行隔离和周转。p97 通过靶向线粒体融合促进因子 mitofusin 进行降解，从而发挥作用，这种降解是通过类似于内质网相关降解（ERAD）的机制进行的。
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