background:
The ILK protein is important in different biological pathways such as cell adhesion, anchorage-dependent cell cycle progression, oncogenic transformation, and growth factor signaling. The kinase activity of ILK is low in non-activated cells; its activity is stimulated by cell-ECM interactions and by certain growth factors. 3 Negative regulation of ILK is mediated by two phosphatases: PTEN, a tumor suppressor lipid sphatase, and ILKAP, a PP2C protein phosphatase. In tumor cells that do not express PTEN protein, ILK is constitutively active.
Function:
Receptor-proximal protein kinase regulating integrin-mediated signal transduction. May act as a mediator of inside-out integrin signaling. Focal adhesion protein part of the complex ILK-PINCH. This complex is considered to be one of the convergence points of integrin- and growth factor-signaling pathway. Could be implicated in mediating cell architecture, adhesion to integrin substrates and anchorage-dependent growth in epithelial cells. Phosphorylates beta-1 and beta-3 integrin subunit on serine and threonine residues, but also AKT1 and GSK3B.
Subunit:
Interacts with cytoplasmic domain of beta 1 subunit of integrin. Could also interacts with beta 2, beta 3 and/or beta 5 subunit of integrin. Interacts (via ANK repeats) with LIMS1 and LIMS2. Interacts with parvins and probably TGFB1I1. Interacts (via ANK repeats) with EPHA1 (via SAM domain); stimulated by EFNA1 but independent of the kinase activity of EPHA1.
Subcellular Location:
Cell junction, focal adhesion. Cell membrane; Peripheral membrane protein; Cytoplasmic side.
Tissue Specificity:
Highly expressed in heart followed by skeletal muscle, pancreas and kidney. Weakly expressed in placenta, lung and liver.
Post-translational modifications:
Autophosphorylated on serine residues.
Similarity:
Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family.
Contains 5 ANK repeats.
Contains 1 protein kinase domain.
Database links:
UniProtKB/Swiss-Prot: Q13418.2
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
ILK 是一种新发现的Ser/Thr蛋白激酶。ILK能够通过与整合素β1亚单位的结合介导细胞与胞外基质的连接,以依赖于PI3K的方式激活,并通过磷酸化下游底物PKB/AKT,GSK3等胞外信号的一项下游传递,对细胞的生长,分化,迁移等进行调控。由于ILK在胞内外信号传导中起着重要的作用。并且抑制ILK的活性能够导致细胞周期的停滞和细胞程序性死亡的启动,使其成为肿瘤治疗和肿瘤药物的理想靶位点。
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