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Technical Data |
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A0005 |
Abl SH2 Domain |
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Description: The v-abl oncogene, which was originally described in the murine Abelson retrovirus, encodes a non-receptor tyrosine kinase that can mediate cell transformation. Mammalian c-Abl is associated with normal cell growth and differentiation, and is distributed in the nucleus, and the cytoplasm in association with F-actin. In the nucleus, c-Abl has been shown to bind chromatin in a cell cycle regulated manner. Deletion of the F-actin binding and the chromatin binding regions of c-Abl has been shown to block cell growth despite the production of an active tyrosine kinase. In chronic myelogenous leukemia (CML), the c-abl protooncogene translocates from chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22 forming the Philadelphia chromosome. This translocation causes the expression of a novel 210kD Abl-Bcr fusion gene product which is only found in malignant cells and is believed to play a crucial role in the pathogenesis of CML. Western Immunoblot Analysis: Tested by using the antibody (1mg/ml) to detect Abl-Bcr (~210kDa) and c-Abl (~140kDa) in human K562 leukemia cells. Note: The amount of c-Abl tends to be low in many cell lines and c-Abl was not detected using RIPA lysates from human Jurkat, Raj and Hut lymphoid cell lines, or murine Wehi myeloid cell line. Immunoprecipitation: Tested by using the antibody (15ug) to immunoprecipitate Abl-Bcr (~210kDa) and c-Abl (~140kDa) from a lysate of human K562 leukemia cells. Storage and Stability: Stable for 1 year at- 20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. |
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