Dissociation of focal adhesion kinase and paxillin tyrosine phosphorylation induced by bombesin and lysophosphatidic acid from epidermal growth factor receptor transactivation in Swiss 3T3 cells.

Salazar EP; Hunger Glaser I; Rozengurt E

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Dissociation of focal adhesion kinase and paxillin tyrosine phosphorylation induced by bombesin and lysophosphatidic acid from epidermal growth factor receptor transactivation in Swiss 3T3 cells.

机译：离解的粘着斑激酶和桩蛋白酪氨酸磷酸化蛙皮素引起的从表皮生长lysophosphatidic酸因子受体transactivation瑞士3 t3细胞。

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Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs). The pathways involved remain incompletely understood. The experiments presented here were designed to test the role of epidermal growth factor receptor (EGFR) transactivation in the rapid increase of tyrosine phosphorylation of FAK and paxillin induced by GPCR agonists. Our results show that treatment with the selective EGFR tyrosine kinase inhibitor AG 1478, at concentrations that completely blocked the increase in tyrosine phosphorylation of these proteins induced by EGF, did not affect the stimulation of tyrosine phosphorylation of either FAK or paxillin induced by multiple GPCR agonists including LPA, BOM, vasopressin, bradykinin, and endothelin. Similar results were obtained when Swiss 3T3 cells were treated with another highly specific inhibitor of the EGF receptor kinase activity, PD-158780. Collectively, our results clearly dissociate EGFR transactivation from the tyrosine phosphorylation of FAK and paxillin induced by multiple GPCR agonists.

机译：nonreceptor酪氨酸磷酸化酪氨酸激酶p125粘着斑激酶(FAK)迅速和适配器蛋白质桩蛋白增加了多种受体激动剂,包括蛙皮素(BOM)和lysophosphatidic酸(LPA),通过heptahelical G protein-coupled受体(GPCRs)。不完全理解。是用来测试的作用表皮生长因子受体(EGFR)transactivation酪氨酸的快速增长FAK磷酸化和桩蛋白引起的GPCR受体激动剂。选择性表皮生长因子受体酪氨酸激酶抑制剂1478年AG浓度完全封锁了酪氨酸磷酸化的增加这些蛋白质通过EGF诱导,没有影响酪氨酸的磷酸化的刺激由多个GPCR FAK或桩蛋白诱导后叶加压素受体激动剂包括LPA、物料清单,缓激肽、内皮素。当瑞士3 t3细胞处理获得的另一个非常具体的表皮生长因子抑制剂受体激酶活性,pd - 158780。总的来说,我们的研究结果清楚地分离表皮生长因子受体transactivation酪氨酸磷酸化由多个GPCR的FAK和桩蛋白诱导受体激动剂。

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来源
《Journal of Cellular Physiology》 |2003年第3期|314-324|共11页
作者
Salazar EP; Hunger Glaser I; Rozengurt E;
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Department of Medicine, School of Medicine and Molecular Biology Institute, University of California, Los Angeles, California 90095-178622, USA.;

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正文语种英语
中图分类细胞生物学;
关键词
Paxillin; Lysophosphatidic Acids; Cytoskeletal ProteinsG-Protein-Coupled ReceptorsTyrosine PhosphorylationSwiss 3T3 CellsProtein-Tyrosine KinasesBombesinErbB ReceptorsPhosphoproteins3T3 CellsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesGenetic Trans-Activationnon-specific protein-tyrosine kinase;

机译：桩蛋白;Lysophosphatidic酸;细胞骨架ProteinsG-Protein-Coupled ReceptorsTyrosinePhosphorylationSwiss 3 t3 CellsProtein-TyrosineKinasesBombesinErbB ReceptorsPhosphoproteins3T3CellsFocal粘附粘着斑激酶1酪氨酸蛋白KinasesGeneticTrans-Activationnon-specific酪氨酸蛋白激酶;

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Dissociation of focal adhesion kinase and paxillin tyrosine phosphorylation induced by bombesin and lysophosphatidic acid from epidermal growth factor receptor transactivation in Swiss 3T3 cells.

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