Inhibition of cell adhesion by xARVCF indicates a regulatory function at the plasma membrane.
Inhibition of cell adhesion by xARVCF indicates a regulatory function at the plasma membrane.
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xARVCF 对细胞粘附的抑制表明质膜具有调节功能。
DOI：
10.1002/dvdy.21651
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Fagotto,François
中科院分区：
文献类型：
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作者：
Reintsch,WolfgangE;Mandato,CraigA;McCrea,PierreD;Fagotto,François
钙粘蛋白的胞质尾被认为调节细胞-细胞粘附的强度和动力学。其调节活性的一部分归因于近膜区，即膜结构域（JMD）及其与p120连环蛋白亚家族成员的相互作用。我们表明，滴定xARVCF，这个家庭的成员，质膜破坏粘附在早期胚胎。粘附可以通过组成性活性Rac的共表达来恢复，这表明细胞内信号传导是粘附表型丧失的主要原因。我们的观察结果表明，招聘p120型连环蛋白质膜的钙粘蛋白胞质尾可能会产生蛋白复合物，积极调节胚胎细胞的粘附“状态”。发展动力学237：2328-2341，2008年。© 2008 Wiley‐利斯公司
The cytoplasmic tail of cadherins is thought to regulate the strength and dynamics of cell–cell adhesion. Part of its regulatory activity has been attributed to a membrane‐proximal region, the juxtamembrane domain (JMD), and its interaction with members of the p120 catenin subfamily. We show that titration of xARVCF, a member of this family, to the plasma membrane disrupts adhesion in the early embryo. Adhesion can be restored by coexpression of constitutively active Rac, suggesting that intracellular signaling is the primary cause in the loss of adhesion phenotype. Our observations suggest that the recruitment of p120 type catenins to the plasma membrane by the cadherin cytoplasmic tail may create protein complexes, which actively modulate the adhesion “status” of embryonic cells. Developmental Dynamics 237:2328–2341, 2008. © 2008 Wiley‐Liss, Inc.