Biological Information | |
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Background Information: | The abl oncogene was initially identified as the viral transforming gene (v-abl) of Abelson murine leukemia virus (A-MuLV), from a chemically thymectomized mouse inoculated with Moloney murine leukemia virus (M-MuLV). The v-abl genome consists of M-MuLV gag sequences fused to mouse c-abl, resulting in the production of phosphoproteins, p160 and p120 gag/c-abl with protein-tyrosine kinase activity, as the major translational products. The abl oncogene is implicated in serval human leukemias including chronic myelocytic (CML), adult acute lymphoblastic (ALL) and pediatric ALL. In these leukemias the c-abl proto-oncogene undergoes a chromosomal translocation producing the Philadelphia chromosome resulting in the fusion of c-abl sequences to the bcr gene of chromosome 22, and the molecular consequences of this translocation is the generation of a chimeric bcr/c-abl mRNA encoding activated abl protein-tyrosine kinase.
GenBank U07563. The recombinant protein contains the amino acid substitution, T315I with reference to U07563. This mutation is reported to elicit resistance to the Abl tyrosine kinase inhibitors STI-571. |
Target Class: | Kinase |
Accession Number: | NM_005157.3; NM_007313.2 |
Target Name: | Abl |
Target Aliases: | ABL1, JTK7, ABL, p150, v-abl, c-ABL, bcr/abl |
Target Species: | Human |
Usage | |
Product Type: | Enzymes |
Application: | Drug Discovery & Development |
Storage Conditions: | 6 months at -70°C |
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Abl (T315I), active
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