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一种新型β1整合素连接蛋白激酶对细胞黏附及锚定依赖性生长的调控

Regulation of cell adhesion and anchorage-dependent growth by a new beta 1-integrin-linked protein kinase.

作者信息

Hannigan G E, Leung-Hagesteijn C, Fitz-Gibbon L, Coppolino M G, Radeva G, Filmus J, Bell J C, Dedhar S

机构信息

Cancer Biology Research Program, Sunnybrook Health Science Centre, University of Toronto, Ontario, Canada.

出版信息

Nature. 1996 Jan 4;379(6560):91-6. doi: 10.1038/379091a0.

Abstract

The interaction of cells with the extracellular matrix regulates cell shape, motility, growth, survival, differentiation and gene expression, through integrin-mediated signal transduction. We used a two-hybrid screen to isolate genes encoding proteins that interact with the beta 1-integrin cytoplasmic domain. The most frequently isolated complementary DNA encoded a new, 59K serine/threonine protein kinase, containing four ankyrin-like repeats. We report here that this integrin-linked kinase (ILK) phosphorylated a beta 1-integrin cytoplasmic domain peptide in vitro and coimmunoprecipitated with beta 1 in lysates of mammalian cells. Endogenous ILK kinase activity was reduced in response to fibronectin. Overexpression of p59ILK disrupted epithelial cell architecture and inhibited adhesion to integrin substrates, while inducing anchorage-independent growth. We propose that ILK is a receptor-proximal protein kinase regulating integrin-mediated signal transduction.

摘要

细胞与细胞外基质的相互作用通过整合素介导的信号转导来调节细胞形状、运动性、生长、存活、分化和基因表达。我们利用双杂交筛选来分离编码与β1整合素胞质结构域相互作用的蛋白质的基因。最常分离到的互补DNA编码一种新的59K丝氨酸/苏氨酸蛋白激酶,含有四个锚蛋白样重复序列。我们在此报告,这种整合素连接激酶(ILK)在体外使β1整合素胞质结构域肽磷酸化,并在哺乳动物细胞裂解物中与β1共同免疫沉淀。内源性ILK激酶活性因纤连蛋白而降低。p59ILK的过表达破坏上皮细胞结构并抑制对整合素底物的黏附,同时诱导不依赖贴壁的生长。我们提出ILK是一种调节整合素介导信号转导的受体近端蛋白激酶。

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