反应种属
Human;Mouse;Rat;Monkey
蛋白名称
Tyrosine-protein kinase ABL1
分子量（DA）
125(200kd BCR-ABL complex）
免疫原
The antiserum was produced against synthesized peptide derived from human Abl around the phosphorylation site of Tyr204. AA range:156-205
特异性
Phospho-Abl1 (Y204) Polyclonal Antibody detects endogenous levels of Abl1 protein only when phosphorylated at Y204.
组成
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
来源
Polyclonal, Rabbit,IgG
稀释比例
WB: 1/500 - 1/2000. IHC: 1/100 - 1/300. ELISA: 1/5000.. IF 1:50-200
纯化工艺
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
其他名称
ABL1; ABL; JTK7; Tyrosine-protein kinase ABL1; Abelson murine leukemia viral oncogene homolog 1; Abelson tyrosine-protein kinase 1; Proto-oncogene c-Abl; p150
背景
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
功能
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
