|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||51419 Da|
|Other Names||Integrin-linked protein kinase, 59 kDa serine/threonine-protein kinase, ILK-1, ILK-2, p59ILK, ILK, ILK1, ILK2|
|Target/Specificity||A synthetic peptide corresponding to residues near N-term of human ILK protein was used as immunogen|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||ILK Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
|Cellular Location||Cell junction, focal adhesion. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Cell projection, lamellipodium. Cytoplasm, myofibril, sarcomere|
|Tissue Location||Highly expressed in heart followed by skeletal muscle, pancreas and kidney. Weakly expressed in placenta, lung and liver|
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Provided below are standard protocols that you may find useful for product applications.
Integrin-linked kinase (ILK) is a key cytoplasmic plaque protein involved in the mediation of integrin functions. It plays a key role as a regulator during cell survival, cell proliferation, cell migration, and cell to cell adhesion (1). ILK links integrins to the actin cytoskeleton, allowing transduction of signals through integrins to the extracellular matrix (ECM). Also, ILK has been linked to the regulation of smooth contraction and cell motility in non-muscle cells through phosphorylation of myosin (2). Irregular activity level of ILK has been linked to expression of certain tumor. ILK overexpression caused by inactivating mutation in tumor suppressors (e.g. PTEN and APC) lead to tumor formation in transgenic mouse. Up-regulated ILK expression and activity are seen in Ewings scaromas, colorectal cancers, and late staged prostate cancers (3).
1. Marotta A et al. Oncogene. 20:6250
2. Wu C et al. J Cell Biol. 155(4):505-10, 2001.
3. Marotta A et al. Oncogene. 20:6250
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