Antibody type
Monoclonal antibodies
Protein name
Tyrosine-protein kinase ABL1
Immunogen
Purified recombinant fragment of c-Abl (aa577-650) expressed in E. Coli.
Specificity
c-Abl Monoclonal Antibody detects endogenous levels of c-Abl protein.
Constitute
Ascitic fluid containing 0.03% sodium azide,0.5% BSA, 50%glycerol.
Dilution rate
Western Blot: 1/500 - 1/2000. ELISA: 1/10000. Not yet tested in other applications.
Purification process
Affinity purification
Other name
ABL1; ABL; JTK7; Tyrosine-protein kinase ABL1; Abelson murine leukemia viral oncogene homolog 1; Abelson tyrosine-protein kinase 1; Proto-oncogene c-Abl; p150
Background
This gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [pr
Function
catalytic activity:ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.,cofactor:Magnesium or manganese.,disease:A chromosomal aberration involving ABL1 is a cause of chronic myeloid leukemia (CML) [MIM:608232]. Translocation t(9;22)(q34;q11) with BCR. The translocation produces a BCR-ABL found also in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).,enzyme regulation:Stabilized in the inactive form by an association between the SH3 domain and the SH2-TK linker region, interactions of the amino-terminal cap, and contributions from an amino-terminal myristoyl group and phospholipids. Activated by autophosphorylation as well as by SRC-family kinase-mediated phosphorylation. Activated by RIN1 binding to the SH2 and SH3 domains. Inhibited by imatinib mesylate (Gleevec) which is used for the treatment of chronic myeloid leukemia (CML).,function:Regulates
