MFN2型
第一季
线粒体融合
MFN1型
线粒体分裂
线粒体
生物
计算生物学
细胞生物学
热休克蛋白A9
DNAJA3公司
遗传学
生物信息学
线粒体DNA
基因
肽序列
作者
Tharsini Navaratnarajah,Ruchika Anand,Andreas S. Reichert,Felix Distelmaier
标识
DOI:10.1016/j.biocel.2021.105951
摘要
Mitochondria are highly dynamic organelles, which undergo frequent structural and metabolic changes to fulfil cellular demands. To facilitate these processes several proteins are required to regulate mitochondrial shape and interorganellar communication. These proteins include the classical mitochondrial fusion (MFN1, MFN2, and OPA1) and fission proteins (DRP1, MFF, FIS1, etc.) as well as several other proteins that are directly or indirectly involved in these processes (e.g. YME1L, OMA1, INF2, GDAP1, MIC13, etc.). During the last two decades, inherited genetic defects in mitochondrial fusion and fission proteins have emerged as an important class of neurodegenerative human diseases with variable onset ranging from infancy to adulthood. So far, no causal treatment strategies are available for these disorders. In this review, we provide an overview about the current knowledge on mitochondrial dynamics under physiological conditions. Moreover, we describe human diseases, which are associated with genetic defects in these pathways.
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