This antibody is predicted to react with Monkey, Horse, Dog and Bat
Recombinant rabbit monoclonal antibodies are produced using in vitro expression systems. The expression systems are developed by cloning in the specific antibody DNA sequences from immunoreactive rabbits. Then, individual clones are screened to select the best candidates for production. The advantages of using recombinant rabbit monoclonal antibodies include: better specificity and sensitivity, lot-to-lot consistency, animal origin-free formulations, and broader immunoreactivity to diverse targets due to larger rabbit immune repertoire.
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. In chronic myelogenous leukemia and a subset of acute lymphoblastic leukemias, the c-Abl proto oncogene undergoes a (9;22) chromosomal translocation producing a novel rearranged chromosome (the Philadelphia chromosome) As the result of the fusion of c-Abl sequences from chromosome 9 to the Bcr gene on chromosome 22. The molecular consequence of this translocation is the generation of a chimeric Bcr/Abl mRNA encoding activated Abl protein tyrosine kinase. The c-Abl oncogene was initially identified as the viral transforming gene of Abelson murine leukemia virus (A-MuLV). The major translational product of c-Abl has been identified as a protein with tyrosine kinase activity and an SH2 domain. 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.
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Protein Aliases: Abelson murine leukemia oncogene; Abelson murine leukemia viral oncogene homolog 1; Abelson tyrosine-protein kinase 1; Abl 1 antib; ABL2; ABLL; ARG; B30; bcr/c-abl oncogene protein; c-abl oncogene 1, receptor tyrosine kinase; p150; Proto-oncogene c-Abl; proto-oncogene tyrosine-protein kinase ABL1; RP11-83J21.1; Tyrosine kinase ARG; Tyrosine-protein kinase ABL1; v-abl Abelson murine leukemia oncogene 1; v-abl Abelson murine leukemia viral oncogene homolog 1
Gene Aliases: ABL; ABL1; AI325092; bcr/abl; c-ABL; c-ABL1; E430008G22Rik; JTK7; p150; v-abl