Focal adhesion disassembly requires clathrin-dependent endocytosis of integrins.

Focal adhesion disassembly requires clathrin-dependent endocytosis of integrins.
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DOI:
10.1016/j.febslet.2009.03.037
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发表时间:
2009-04-17
期刊:
影响因子:
3.5
通讯作者:
Kunz, Jeannette
Kunz, Jeannette
中科院分区:
生物学3区
文献类型:
--
作者:
Chao, Wei-Ting;Kunz, Jeannette

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细胞迁移需要局部粘连的可控分解,但其潜在的机制仍然知之甚少。在这里,我们表明黏附转换是通过依赖动力蛋白和笼蛋白的激活的β1整合素的内吞作用来调节的。与此一致的是,在黏附解离之前,网状蛋白和网状蛋白接头AP-2和失活的-2(DAB2)与动力素2一起分布到黏附部位。此外,Dynamin 2或两者都被敲除会阻止β1整合素的内化,导致局部黏附分解和细胞迁移受损。综上所述,这些结果为了解黏附解离的机制和识别解离途径的新成分提供了重要的见解。
Cell migration requires the controlled disassembly of focal adhesions, but the underlying mechanisms remain poorly understood. Here, we show that adhesion turnover is mediated through dynamin- and clathrin-dependent endocytosis of activated β1 integrins. Consistent with this, clathrin and the clathrin adaptors AP-2 and disabled-2 (DAB2) distribute along with dynamin 2 to adhesion sites prior to adhesion disassembly. Moreover, knockdown of either dynamin 2 or both clathrin adaptors blocks β1 integrin internalization, leading to impaired focal adhesion disassembly and cell migration. Together, these results provide important insight into the mechanisms underlying adhesion disassembly and identify novel components of the disassembly pathway.
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