De novo expression of pp125FAK in human macrophages regulates CSK distribution and MAP kinase activation but does not affect focal contact structure.

De Nichilo-MO; Katz BZ; OConnell BYamada KM

首页> 外文期刊>Journal of Cellular Physiology >De novo expression of pp125FAK in human macrophages regulates CSK distribution and MAP kinase activation but does not affect focal contact structure.

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De novo expression of pp125FAK in human macrophages regulates CSK distribution and MAP kinase activation but does not affect focal contact structure.

机译：新创pp125FAK在人类的表情巨噬细胞调节埋头分布和地图激酶激活但不影响焦联系结构。

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The protein tyrosine kinase pp125FAK (focal adhesion kinase, or FAK) is expressed by a variety of cell types and has been implicated in integrin-mediated signaling events. We explored the potential functions of FAK by expressing it de novo in a cell type lacking FAK. We showed previously that cultured human macrophages lack FAK yet still have well-formed focal contacts. Adenovirus-mediated expression of FAK results in the appearance of FAK protein, which localizes to focal contacts and becomes tyrosine-phosphorylated without perturbing overall cell morphology or focal contacts. FAK associates with CSK 48 h after infection and recruits it to focal contacts. Tyrosine phosphorylation of p130cas but not of paxillin is stimulated after FAK expression. The phosphorylation of p130cas is lost at 48 h in parallel with CSK accumulation in focal contacts. The ERK2 form of MAP kinase is similarly activated at 12-24 h, but it also returns to low levels at 48 h. These findings demonstrate that FAK can be reconstituted to focal contacts in cells that lack it without affecting cell morphology or focal contact structure. FAK can regulate the distribution and activities of elements of the MAP kinase signaling pathway.

机译：蛋白质酪氨酸激酶pp125FAK(焦黏附激酶或FAK)由一个表示多种细胞类型和被卷入integrin-mediated信号事件。FAK的表达的潜在功能细胞类型缺乏FAK新创。以前,人工培养的巨噬细胞所缺乏的FAK但仍有格式良好的焦联系人。Adenovirus-mediated FAK的表达结果FAK蛋白的出现,定位焦接触,成为没有干扰酪氨酸磷酸化整体细胞形态学或焦联系人。同事埋头在感染后48 h和新兵焦接触。的磷酸化p130cas但不是桩蛋白刺激后FAK的表达。的磷酸化p130cas丢失在48小时与埋头在焦接触积累。ERK2的MAP激酶是类似的激活在12 - 24 h,但也回报低水平48 h。这些发现证明可以重组FAK焦接触细胞缺乏它不影响细胞形态或焦接触结构。规范的分布和活动MAP激酶信号通路的元素。

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来源
《Journal of Cellular Physiology》 |1999年第2期|164-172|共9页
作者
De Nichilo-MO; Katz BZ; OConnell BYamada KM;
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作者单位

Craniofacial Developmental Biology and Regeneration Branch, NIDCR, NIH, Bethesda, Maryland 20892-4370, USA.;

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原文格式 PDF
正文语种英语
中图分类细胞生物学;
关键词
contact configuration; Focal Adhesions; PTK2 wt AlleleFocal Adhesion Kinase 1Cell Adhesion MoleculesMitogen-Activated Protein Kinasescell morphologycell type;

机译：接触配置;焦粘连;PTK2 wtAlleleFocal黏附激酶1细胞粘附MoleculesMitogen-Activated蛋白质Kinasescellmorphologycell类型;

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De novo expression of pp125FAK in human macrophages regulates CSK distribution and MAP kinase activation but does not affect focal contact structure.

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