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DOK2 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | O60496 |
|---|---|
| Clone Names | 2072402 |
| Gene ID | 9046 |
|---|---|
| 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 AP7691b was selected from the C-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 | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| 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. |
| Name | DOK2 |
|---|---|
| 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.
Background
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.
References
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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