Kindlin-2 controls bidirectional signaling of integrins
Kindlin-2 controls bidirectional signaling of integrins
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DOI：
10.1101/gad.469408
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发表时间：
2008-05-15
影响因子：
10.5
通讯作者：
Faessler, Reinhard
中科院分区：
文献类型：
--
作者：
Montanez, Eloi;Ussar, Siegfried;Faessler, Reinhard
细胞粘附和配体诱导的信号传导需要控制整合素的激活。本研究报告了小鼠局灶黏附蛋白Kindlin-2的缺失导致内胚层和外胚层严重脱离基底膜而导致着床期死亡。我们发现Kindlin-2缺陷的细胞不能激活它们的整合素，而Kindlin-2是talin诱导的整合素激活所必需的。此外，我们证明了kindin -2是整合素外向内信号传导所必需的，以实现牢固的粘附和扩散。我们的研究结果提供了证据，证明Kindlin-2是双向整合素信号传导的一个新的和必要的元素。
Control of integrin activation is required for cell adhesion and ligand-induced signaling. Here we report that loss of the focal adhesion protein Kindlin-2 in mice results in peri-implantation lethality caused by severe detachment of the endoderm and epiblast from the basement membrane. We found that Kindlin-2-deficient cells were unable to activate their integrins and that Kindlin-2 is required for talin-induced integrin activation. Furthermore, we demonstrate that Kindlin-2 is required for integrin outside-in signaling to enable firm adhesion and spreading. Our findings provide evidence that Kindlin-2 is a novel and essential element of bidirectional integrin signaling.