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Overview
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Background
Dok-1 associates with the Ras GTPase activating protein (Ras GAP) upon tyrosine phosphorylation. Evidence suggests that p62 Dok-1 is a substrate of the constitutive tyrosine kinase activity of p210 Bcr-Abl, a fusion protein caused by the t(9;22) translocation and associated with chronic myelogenous leukemia. Dok-1, as well as the tyrosine kinase substrates IRS-1 and Cas, is a member of a class of “docking” proteins which contain multiple tyrosine residues and putative SH2 binding sites. Dok-1 is suspected to be the substrate phosphorylated in response to stimulation by a number of growth factors, including PDGF, VEGF, insulin and IGF. Dok-2 (also designated p56 Dok) has also been identified as a potential mediator of the effects of p210 Bcr-Abl.
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