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首页> 外文期刊>Genes to cells : >Cdc42 and Rac small G proteins activated by trans-interactions of nectins are involved in activation of c-Jun N-terminal kinase, but not in association of nectins and cadherin to form adherens junctions, in fibroblasts.
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Cdc42 and Rac small G proteins activated by trans-interactions of nectins are involved in activation of c-Jun N-terminal kinase, but not in association of nectins and cadherin to form adherens junctions, in fibroblasts.

机译：通过果胶的反式相互作用激活的Cdc42和Rac小G蛋白参与c-Jun N末端激酶的激活，但不参与果胶和钙粘蛋白的结合，从而在成纤维细胞中形成粘附连接。

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BACKGROUND: Nectins are Ca2+-independent immunoglobulin-like cell-cell adhesion molecules which associate with cadherins to form adherens junctions (AJs) in epithelial cells and fibroblasts. Nectin-1 and -3 are members of the nectin family which most strongly trans-interact, causing cell-cell adhesion. The trans-interaction between nectin-1 and -3 induces the activation of both Cdc42 and Rac small G proteins in epithelial cells. We studied the roles of Cdc42 and Rac activated in this way in L fibroblasts stably expressing both nectin-1 and E-cadherin (nectin-1-EL cells). RESULTS: The trans-interaction between nectin-1 and -3 induced the activation of Cdc42 and Rac in nectin-1-EL cells. Cdc42, and presumably Rac, activated in this way, induced the activation of c-Jun N-terminal kinase (JNK), but not p38 mitogen-activated protein (MAP) kinase or extracellular signal-regulated kinase (ERK). Cdc42 or Rac was not essential for the association of nectin-1 and E-cadherin to form AJs. Reorganization of the actin cytoskeleton was not required for the association of nectin-1 and E-cadherin. CONCLUSION: These results indicate that Cdc42 and Rac activated by the trans-interaction of nectins selectively induce the activation of JNK, but are not essential for the association of nectins and cadherin to form AJs in fibroblasts.
机译：背景：凝集素是独立于Ca2 +的免疫球蛋白样细胞粘附分子，与钙粘蛋白结合形成上皮细胞和成纤维细胞的粘附连接（AJs）。 Nectin-1和-3是Nectin家族的成员，它们之间的相互作用最强，引起细胞粘附。 nectin-1和-3之间的反式相互作用诱导上皮细胞中Cdc42和Rac小G蛋白的激活。我们研究了以这种方式激活的Cdc42和Rac在稳定表达nectin-1和E-cadherin（nectin-1-EL细胞）的L成纤维细胞中的作用。结果：nectin-1和-3之间的反式相互作用诱导了nectin-1-EL细胞中Cdc42和Rac的活化。以这种方式激活的Cdc42和大概是Rac诱导了c-Jun N末端激酶（JNK）的激活，但未诱导p38丝裂原激活的蛋白（MAP）激酶或细胞外信号调节激酶（ERK）的激活。 Cdc42或Rac对于nectin-1和E-cadherin形成AJ的结合不是必需的。 Nectin-1和E-cadherin的缔合不需要肌动蛋白细胞骨架的重组。结论：这些结果表明，通过果胶的反式相互作用激活的Cdc42和Rac选择性地诱导JNK的激活，但对于果胶和钙粘蛋白的结合在成纤维细胞中形成AJ并不是必需的。

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