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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Paxillin αand Crk-associated substrate exert opposing effects on cell migration and contact inhibition of growth through tyrosine phosphorylation
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Paxillin αand Crk-associated substrate exert opposing effects on cell migration and contact inhibition of growth through tyrosine phosphorylation

机译：Paxillinα和Crk相关底物通过酪氨酸磷酸化对细胞迁移和生长的接触抑制产生相反的作用

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摘要

Protein tyrosine phosphorylation accompanies and is essential for integrin signaling. We have shown that tyrosine phosphorylation of paxillin αand Crk-associated substrate (p130~Cas) is a prominent event on integrin activation in normal murine mammary qland epithelial cells. Tyrosine phosphorylation of p130~Cas has been demonstrated to facilitate cell migration. We show here that tyrosine phosphorylation of paxillin αacts to reduce haptotactic cell migrations as well as transcellular invasive activities in several different experimental cell systems, whereas tyrosine phosphory- lation of p130~Cas exerts opposing effects to those of paxillin o. Each of the phosphorylation-null mutants acts as a dominant negative for each phenotype. Moreover, we found that overexpression of paxillin αreduced the cell saturation density of normal murine mammary gland cells, whereas overexpression of p130~Cas in- creased it. These effects also seemed to depend on tyrosine phosphorylation events. Cell growth rates and morphologies at growing phases were not significantly altered, nor were cells transformed. Addition of epidermal growth factor increased sat- uration density of the paxillin α-overexpressing cells, whereas no further increment was observed in p130~Cas-overexpressing cells. We propose that tyrosine phosphorylation of paxillin αand p130~Cas exerts opposing effects on several integrin-mediated cellular events. possibly through different signaling pathways.
机译：蛋白质酪氨酸磷酸化伴随并整合素信号转导必不可少。我们已经证明，在正常小鼠乳腺qland上皮细胞中，整合素激活时，paxillinα和Crk相关底物（p130〜Cas）的酪氨酸磷酸化是一个重要事件。 p130〜Cas的酪氨酸磷酸化已被证明有助于细胞迁移。我们在这里表明，在一些不同的实验细胞系统中，paxillinα的酪氨酸磷酸化可减少触觉细胞迁移以及跨细胞侵袭活性，而p130〜Cas的酪氨酸磷酸化则与paxillin o产生相反的作用。每个磷酸化无效突变体充当每种表型的显性阴性。此外，我们发现Paxillinα的过表达降低了正常鼠乳腺细胞的细胞饱和密度，而p130〜Cas的过表达则使之升高。这些作用似乎也取决于酪氨酸磷酸化事件。细胞在生长阶段的生长速率和形态没有明显改变，细胞也没有转化。表皮生长因子的添加增加了Paxillinα过表达细胞的饱和密度，而在p130〜Cas过表达细胞中未观察到进一步的增加。我们认为，paxillinα和p130〜Cas的酪氨酸磷酸化对多种整合素介导的细胞事件起相反的作用。可能通过不同的信号通路。

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