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The mutation was confirmed by LC-MS/MS using digestion with Trypsin.
For maximum recovery please spin prior to use. Unless noted below, aliquots of the 5 µg, 10 µg and 20 µg sizes of kinase are not recommended as materials can be used in original packaging until exhausted. For larger sizes, the number of freeze/thaws may be reduced by preparing aliquots; aliquots below 20 µL are not recommended. Please never store a kinase diluted. If properly stored at -80C, this product is guaranteed for 6 months from date of purchase.
Protein Form: Full Length
c-Abl (Abelson murine leukemia viral oncogene homolog 1, ABL1) is a 140 kDa proto-oncogene member of the Src family of non-receptor tyrosine kinases. c-Abl has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns c-Abl into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR and c-Abl genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for c-Abl. The c-Abl oncogene is implicated in several human leukemias including 90-95% of chronic myelocytic leukemia (CML), 20-25% of adult acute lymphoblastic leukemia (ALL) and 2-5% of pediatric ALL. c-Abl localizes to dynamic actin structures, and phosphorylates CRK and CRKL, DOK1, and other proteins controlling cytoskeleton dynamics. c-ABL potentially regulates DNA repair by activating the proapoptotic pathway when the DNA damage is too severe to be repaired.
仅用于科研。不用于诊断过程。未经明确授权不得转售。