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Product Details
PV3864
Species
Expression System
Amino acid sequence
Tag
Molecular weight
Class
Type
Conjugate
Form
Concentration
Purification
Storage buffer
Contains
Storage conditions
Shipping conditions
Product Specific Information
The mutation was confirmed by LC-MS/MS using digestion with Glu-C.
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
Target Information
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
References (0)
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