超越内质网：Ubx2 调控 TOM 复合物介导入核。
Beyond ER: Regulating TOM-Complex-Mediated Import by Ubx2.
机构信息
McGill Parkinson Program, Neurodegenerative Diseases Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
McGill Parkinson Program, Neurodegenerative Diseases Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
出版信息
Trends Cell Biol. 2019 Sep;29(9):687-689. doi: 10.1016/j.tcb.2019.07.003. Epub 2019 Jul 26.
Despite the progress in understanding the molecular responses to mitochondrial damage, responses to aberrant accumulation of mitochondrial precursor proteins and mitochondrial import defects remain poorly understood. Recent work (Mårtensson et al., Nature, 2019) has unveiled a pathway similar to endoplasmic-reticulum-associated degradation (ERAD) in fine-tuning the fidelity of translocase of the outer mitochondrial membrane (TOM) complex-mediated mitochondrial import.
尽管人们在理解线粒体损伤的分子反应方面取得了进展，但对于线粒体前体蛋白异常积累和线粒体导入缺陷的反应仍知之甚少。最近的研究（Mårtensson 等人，《自然》，2019）揭示了一条类似于内质网相关降解（ERAD）的途径，可微调外膜转位酶（TOM）复合物介导的线粒体导入的保真度。
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