线粒体分裂：分子机制与生理功能。
Mitochondrial division: molecular machinery and physiological functions.
机构信息
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
出版信息
Curr Opin Cell Biol. 2011 Aug;23(4):427-34. doi: 10.1016/j.ceb.2011.04.009. Epub 2011 May 10.
Abstract
Mitochondrial division has emerged as a key mechanism for this essential organelle to maintain its structural integrity, intracellular distribution, and functional competence. An evolutionarily conserved dynamin-related GTPase, Dnm1p/Drp1, interacts with other proteins to form the core machinery involved in mitochondrial division. We summarize recent progress in understanding how the division machinery assembles onto mitochondria and how mitochondrial division contributes to cellular physiology and human diseases.
摘要
线粒体分裂作为一种关键机制，可维持该细胞器的结构完整性、细胞内分布和功能能力。一种进化上保守的与 dynamin 相关的 GTP 酶，Dnm1p/Drp1，与其他蛋白质相互作用，形成参与线粒体分裂的核心机器。我们总结了近期在理解分裂机器如何组装到线粒体以及线粒体分裂如何促进细胞生理学和人类疾病方面的进展。
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本文引用的文献
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Mff is an essential factor for mitochondrial recruitment of Drp1 during mitochondrial fission in mammalian cells.Mff 是哺乳动物细胞中线粒体分裂过程中 Drp1 招募到线粒体所必需的因素。
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Molecular architecture of a dynamin adaptor: implications for assembly of mitochondrial fission complexes.一种动力蛋白衔接蛋白的分子结构：对线粒体裂变复合物组装的影响。
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Aberrant mitochondrial fission in neurons induced by protein kinase C{delta} under oxidative stress conditions in vivo.体内氧化应激条件下蛋白激酶 C{delta}诱导神经元中线粒体的异常分裂。
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Mitochondrial fission and cristae disruption increase the response of cell models of Huntington's disease to apoptotic stimuli.线粒体裂变和嵴结构破坏增加亨廷顿病细胞模型对凋亡刺激的反应。
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