|Other Names||Docking protein 2, Downstream of tyrosine kinase 2, p56(dok-2), DOK2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7691a was selected from the N-term region of human DOK2 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||DOK proteins are enzymatically inert adaptor or scaffolding proteins. They provide a docking platform for the assembly of multimolecular signaling complexes. DOK2 may modulate the cellular proliferation induced by IL-4, as well as IL-2 and IL-3. May be involved in modulating Bcr-Abl signaling. Attenuates EGF-stimulated MAP kinase activation (By similarity).|
|Tissue Location||Highly expressed in peripheral blood leukocytes, lymph nodes and spleen. Lower expression in thymus, bone marrow and fetal liver.|
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Provided below are standard protocols that you may find useful for product applications.
Docking proteins interact with receptor tyrosine kinases and mediate particular biological responses using signal transduction. Dok-2 acts as a multiple docking protein downstream of receptor or non-receptor tyrosine kinases. By this mechanism it acts to negatively regulate signal transduction and cell proliferation controlled by cytokines in a feedback loop. Dok-2 is highly expressed in cells and tissues of hematopoietic origin as well as in lung. Expression of bcr/abl induces additional tyrosine phosphorylation of the Dok1 and Dok2 proteins and their association with Ras-GAP. Thus, it is suspected that DOK association regulates GAP activity toward Ras and that the Dok proteins serve as mediators of bcr-abl signaling. The role of Dok proteins in bcr-abl regulation may also be implicated in chronic myelogenous leukemia (CML), which is characterized by a Philadelphia chromosome translocation t(9;22). Such a mutation would result in a p210-bcr/abl chimeric protein-tyrosine kinase which has been found in many CML cases.
Salomon, A.R., et al., Proc. Natl. Acad. Sci. U.S.A. 100(2):443-448 (2003).Di Cristofano, A., et al., J. Biol. Chem. 273(9):4827-4830 (1998).
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