TSPO interacts with VDAC1 and triggers a ROS-media

TSPO interacts with VDAC1 and triggers a ROS-mediated inhibition of mitochondrial quality control 期刊名称： Autophagy

gsm模块作者： Gatliff, Jemma, East, Daniel, Crosby, James, Abeti, Rosella, Harvey, Robert,高频发生器

Craigen, William, Parker, Peter, Campanella, Michelangelo

年份： 2014年钢领

压铁饼期号：第12期

关键词： mitochondria; mitophagy; PARK2; ROS; TSPO; ubiquitin

摘要：The 18-kDa TSPO (translocator protein) localizes on the outer mitochondrial membrane (OMM) and participates in cholesterol transport. Here, we report that TSPO inhibits mitochondrial autophagy downstream of the PINK1-PARK2 pathway, preventing essential ubiquitination of proteins. TSPO abolishes mitochondrial relocation of SQSTM1/p62 (sequestosome 1), and consequently that

of the autophagic marker LC3 (microtubule-associated protein 1 light chain 3), thus leading to an accumulation of dysfunctional mitochondria, altering the appearance

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of the network. Independent of cholesterol regulation, the modulation of mitophagy by TSPO is instead dependent on VDAC1 (voltage-dependent anion channel 1), to which TSPO binds, reducing mitochondrial coupling and promoting an overproduction of reactive oxygen species (ROS) that 保安对讲机

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