FAK regulates tyrosine phosphorylation of CAS, paxillin, and PYK2 in cells expressing v-Src, but is not a critical determinant of v-Src transformation.

Roy S; Ruest PJ; Hanks SK

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FAK regulates tyrosine phosphorylation of CAS, paxillin, and PYK2 in cells expressing v-Src, but is not a critical determinant of v-Src transformation.

机译：FAK调节表达v-Src的细胞中CAS，paxillin和PYK2的酪氨酸磷酸化，但不是v-Src转化的关键决定因素。

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FAK (focal adhesion kinase) is a nonreceptor protein-tyrosine kinase activated by tyrosine phosphorylation following integrin-mediated cell adhesion. Oncogenic Src promotes enhanced and deregulated FAK tyrosine phosphorylation which has been proposed to contribute to altered cell growth and/or morphological properties associated with transformation. In this study, an inducible FAK expression system was used to study the potential role of FAK in v-Src transformation. Our results portray FAK as a major v-Src substrate that also plays a role in recruiting v-Src to phosphorylate substrates CAS (Crk-associated substrate) and paxillin. The FAK Tyr-397 autophosphorylation site was necessary for this scaffolding function, but was not required for v-Src to stably interact with and phosphorylate FAK. FAK was also shown to negatively regulate v-Src mediated phosphorylation of the FAK-related kinase PYK2. Despite these effects, FAK does not play an essential role in targeting v-Src to major cellular substrates including CAS and paxillin. Nor is FAK strictly required to achieve the altered morphological and growth characteristics of v-Src transformed cells.

机译：FAK（局灶性粘附激酶）是一种非受体蛋白酪氨酸激酶，在整合素介导的细胞粘附后被酪氨酸磷酸化激活。致癌的Src促进增强和失控的FAK酪氨酸磷酸化，已提出其有助于改变细胞生长和/或与转化相关的形态学特性。在这项研究中，使用诱导型FAK表达系统来研究FAK在v-Src转化中的潜在作用。我们的结果将FAK描绘为主要的v-Src底物，它在募集v-Src以磷酸化底物CAS（与Crk相关的底物）和paxillin中也发挥了作用。 FAK Tyr-397自磷酸化位点对于此支架功能是必需的，但对于v-Src与FAK稳定相互作用并使其磷酸化则不是必需的。 FAK还显示出负调控FAK相关激酶PYK2的v-Src介导的磷酸化。尽管有这些作用，FAK在将v-Src靶向主要的细胞底物（包括CAS和Paxillin）方面并未发挥重要作用。也不完全需要FAK来实现v-Src转化细胞形态和生长特性的改变。

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《Journal of cellular biochemistry.》 |2002年第2期|共12页
作者
Roy S; Ruest PJ; Hanks SK;
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正文语种 eng
中图分类细胞生物化学;
关键词
Cytoskeletal Proteins; Oncogene Protein pp60(v-src); Phosphoproteins; Protein-Tyrosine Kinase; 细胞支架蛋白质类; 癌基因蛋白质PP60(V-SRC); 磷蛋白类; 蛋白质酪氨酸激酶;

机译：Cytoskeletal Proteins;Oncogene Protein pp60(v-src);Phosphoproteins;Protein-Tyrosine Kinase;细胞支架蛋白质类;癌基因蛋白质PP60(V-SRC);磷蛋白类;蛋白质酪氨酸激酶;

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1. FAK regulates tyrosine phosphorylation of CAS, paxillin, and PYK2 in cells expressing v-Src, but is not a critical determinant of v-Src transformation. [J] . Roy S, Ruest PJ, Hanks SK Journal of cellular biochemistry. . 2002,第2期

机译：FAK调节表达v-Src的细胞中CAS，paxillin和PYK2的酪氨酸磷酸化，但不是v-Src转化的关键决定因素。
2. Ionizing radiation modules of the expression and tyrosine phosphorylation of the focal adhesion-associated proteins focal adhesion kinase (FAK) and its substrates p130cas and paxillin in A549 human lung carcinoma cells in vitro. [J] . Beinke C, Van Beuningen D, Cordes N International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations . 2003,第9期

机译：电离辐射模块在体外对A549人肺癌细胞中黏着斑相关蛋白局灶性粘附激酶（FAK）及其底物p130cas和paxillin的表达和酪氨酸磷酸化的影响。
3. PKC-regulated myogenesis is associated with increased tyrosine phosphorylation of FAK, Cas, and paxillin, formation of Cas-CRK complex, and JNK activation. [J] . Goel HL, Dey CS Differentiation: The Journal of the International Society of Differentiation . 2002,第6期

机译：PKC调控的肌发生与FAK，Cas和paxillin的酪氨酸磷酸化增加，Cas-CRK复合物的形成以及JNK活化有关。
4. miR-292-5p,let-7g Regulating Protein Kinase C ,Effecting β-casine Expression in Murine Mammary Epithelial Cell [C] . ChunMei Wang, QingZhang Li, Xuejun Gao 奶牛营养与牛奶质量国际研讨会(ist International Symposium on Dairy Cow Nutrition and Milk Quality) . 2009

机译：miR-292-5p，let-7g调节蛋白激酶C，影响小鼠乳腺上皮细胞中β-酪氨酸的表达
5. FcepsilonRI ubiquitylation negatively regulates receptor tyrosine phosphorylation and mast cell effector function. [D] . Billingsley, James Michael. 2006

机译：FcepsilonRI泛素化负调节受体酪氨酸磷酸化和肥大细胞效应子功能。
6. Cellular aging is a critical determinant of primary cell resistance to v-src transformation. [O] . N Tavoloni, H Inoue 1997

机译：细胞老化是原代细胞对v-src转化的抗性的关键决定因素。
7. Induced Focal Adhesion Kinase (FAK) Expression in FAK-Null Cells Enhances Cell Spreading and Migration Requiring Both Auto- and Activation Loop Phosphorylation Sites and Inhibits Adhesion-Dependent Tyrosine Phosphorylation of Pyk2 [O] . Owen, James D., Ruest, Paul J., Fry, David W., 1999

机译：在FAK空细胞中诱导的局灶性粘附激酶（FAK）表达增强细胞的扩散和迁移，需要自动和激活环磷酸化位点，并抑制Pyk2的粘附依赖性酪氨酸磷酸化。

FAK regulates tyrosine phosphorylation of CAS, paxillin, and PYK2 in cells expressing v-Src, but is not a critical determinant of v-Src transformation.

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