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Regulation of JMY's actin nucleation activity by TTC5/STRAP and LC3 during autophagy.
Autophagy ( IF 13.3 ) Pub Date : 2019-01-06 , DOI: 10.1080/15548627.2018.1564417
Xu Liu 1 , Daniel J Klionsky 1
Affiliation  

Actin plays indispensable roles in autophagosome biogenesis. Branched actin networks assembled within phagophore membranes are required for generating the autophagosome membrane shape and movement. The ARP2/3 complex and its regulators, such as JMY (junction mediating and regulatory protein, p53 cofactor), translocate to phagophore membranes to promote local actin filament formation during autophagy. Hu et al., recently showed that during autophagy LC3 recruits JMY to the phagophore and promotes its actin nucleation activity. They also characterized TTC5/STRAP (tetratricopeptide repeat domain 5) as a negative autophagy regulator via binding to JMY and antagonizing its activation. Moreover, an in vitro reconstitution system was developed to demonstrate that membrane-bound LC3 is sufficient to recruit JMY and stimulate JMY-mediated actin filament assembly.

中文翻译:

自噬过程中TTC5 / STRAP和LC3对JMY肌动蛋白成核活性的调节。

肌动蛋白在自噬生物发生中起着不可或缺的作用。组装在吞噬细胞膜内的分支肌动蛋白网络是产生自噬体膜形状和运动所必需的。ARP2 / 3复合物及其调节剂(例如JMY(连接介导和调节蛋白,p53辅因子))易位至吞噬膜,从而促进自噬过程中局部肌动蛋白丝的形成。Hu等人最近表明,在自噬过程中,LC3将JMY募集到了荧光团并促进了其肌动蛋白的成核活性。他们还通过与JMY结合并拮抗其激活,将TTC5 / STRAP(四肽重复序列域5)表征为负自噬调节剂。此外,
更新日期:2019-01-06
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