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膜修复:突触结合蛋白VII持续发挥关键作用。

Membrane resealing: synaptotagmin VII keeps running the show.

作者信息

Andrews Norma W

机构信息

Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA.

出版信息

Sci STKE. 2005 May 3;2005(282):pe19. doi: 10.1126/stke.2822005pe19.

Abstract

Ca2+ influx, an immediate consequence of plasma membrane disruption, triggers a resealing mechanism involving exocytosis. Although this has been known for about a decade, a better understanding of the organelles involved and of the molecular machinery controlling membrane repair has been slower to emerge. Recent studies have changed this picture, by identifying lysosomes as exocytotic vesicles involved in membrane resealing and the Ca2+-binding protein synaptotagmin VII as a regulator of this process. New evidence reinforces the role of the C2A and C2B domains of synaptotagmin VII in plasma membrane repair, highlighting the importance of this molecule as a powerful tool for future studies.

摘要

钙离子内流是质膜破坏的直接后果,它触发了一种涉及胞吐作用的重新封闭机制。尽管这一点已为人所知约十年,但对于所涉及的细胞器以及控制膜修复的分子机制的深入理解却出现得较为缓慢。最近的研究改变了这一局面,通过鉴定溶酶体为参与膜重新封闭的胞吐小泡,并确定钙离子结合蛋白突触结合蛋白VII为这一过程的调节因子。新证据强化了突触结合蛋白VII的C2A和C2B结构域在质膜修复中的作用,凸显了该分子作为未来研究有力工具的重要性。

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