ESCRT puts its thumb on the nanoscale: Fixing tiny holes in endolysosomes.

ESCRT puts its thumb on the nanoscale: Fixing tiny holes in endolysosomes.
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DOI:
10.1016/j.ceb.2020.06.002
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发表时间:
2020-08
影响因子:
7.5
通讯作者:
Hanson PI
Hanson PI
中科院分区:
生物学2区
文献类型:
--
作者:
Bohannon KP;Hanson PI

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ESCRT(转运所需的内体复合物)机制重塑膜,使囊泡从细胞质中出芽。除了这一经典作用外,ESCRT现在被认为可以修复质膜、核膜和整个内溶酶体网络中的损伤。内溶酶体膜的创伤是由病原体、微粒和其他化学或代谢应激引起的。这些膜中的纳米级损伤促进了ESCRT蛋白的激活和参与。对损伤信号、分子传感和膜修复机制的全面理解还有待于发展。然而,钙和ESCRT-I在招募ESCRT-III机制进行膜重塑中的触发作用是这种反应的功能研究中反复出现的主题。在我们目前对脂双层损伤的细胞反应连续体的理解中,ESCRT机制是快速、灵敏的,并且独立于其他系统部署。
The ESCRT (endosomal complex required for transport) machinery remodels membranes to bud vesicles away from the cytoplasm. In addition to this classic role, ESCRTs are now understood to repair damage in the plasma membrane, nuclear envelope, and throughout the endolysosomal network. Wounds in endolysosomal membranes are caused by pathogens, particulates, and other chemical or metabolic stresses. Nanoscale damage in these membranes promotes activation and engagement of ESCRT proteins. A full understanding of damage signals, molecular sensing, and the mechanism of membrane repair has yet to be developed. Nevertheless, a triggering role for calcium and ESCRT-I in recruiting ESCRT-III machinery for membrane remodeling is a repeated theme in functional studies of this response. In our current understanding of the continuum of cellular responses to lipid bilayer damage, the ESCRT machinery is fast, sensitive, and deployed independently of other systems.
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