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慢性收缩活动对骨骼肌线粒体 TOM 复合物组装的可塑性。

Plasticity of TOM complex assembly in skeletal muscle mitochondria in response to chronic contractile activity.

机构信息

Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3.

出版信息

Mitochondrion. 2012 Mar;12(2):305-12. doi: 10.1016/j.mito.2011.11.005. Epub 2011 Nov 25.

Abstract

We investigated the assembly of the TOM complex within skeletal muscle under conditions of chronic contractile activity-induced mitochondrial biogenesis. Tom40 import into mitochondria was increased by chronic contractile activity, as was its time-dependent assembly into the TOM complex. These changes coincided with contractile activity-induced augmentations in the expression of key protein import machinery components Tim17, Tim23, and Tom22, as well as the cytosolic chaperone Hsp90. These data indicate the adaptability of the TOM protein import complex and suggest a regulatory role for the assembly of this complex in exercise-induced mitochondrial biogenesis.

摘要

我们研究了在慢性收缩活动诱导的线粒体生物发生条件下,TOM 复合物在骨骼肌中的组装情况。慢性收缩活动增加了 Tom40 向线粒体的输入,同时也使其在时间上组装成 TOM 复合物。这些变化与收缩活动诱导的关键蛋白输入机械组件 Tim17、Tim23 和 Tom22 以及胞质伴侣 Hsp90 的表达增加相一致。这些数据表明 TOM 蛋白输入复合物具有适应性,并表明该复合物的组装在运动诱导的线粒体生物发生中具有调节作用。

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