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The Abl family of non-receptor tyrosine kinases includes c-Abl (Abelson tyrosine kinase) and Arg (Abl2) subtypes. c-Abl is localized at many subcellular sites including the nucleus, cytoplasm, mitochondria and endoplasmic reticulum, where it interacts with several proteins.
|Cat No||Product Name / Activity|
|p210bcr/abl kinase inhibitor|
|Potent multi-kinase and pan-Bcr-Abl inhibitor|
|Dual Src-Abl inhibitor; antiproliferative|
|Selective allosteric inhibitor of Bcr-Abl tyrosine kinase activity|
|Selective allosteric inhibitor of Bcr-Abl; analog of GNF 2 (Cat. No. 4399)|
|Potent and selective v-Abl tyrosine kinase inhibitor; also inhibits PDGFR and c-kit|
|Inhibitor of c-Abl, v-Src and c-Fyn|
|p210Bcr/Abl kinase inhibitor; also inhibits c-Src and KIT|
|Potent inhibitor of Abl T315l mutant and wild-type Abl kinases|
The Abl family of non-receptor tyrosine kinases includes c-Abl (Abelson tyrosine kinase) and Arg (Abl2) subtypes. c-Abl is localized at several subcellular sites including the nucleus, cytoplasm, mitochondria and endoplasmic reticulum, where it interacts with a large variety of cellular proteins including signaling adaptors, kinases, phosphatases, cell cycle regulators, transcription factors and cytoskeletal proteins.
Due to its diverse range of targets, c-Abl has been implicated in many cellular processes including regulation of cell growth and survival, oxidative stress and DNA-damage responses, and actin dynamics and cell migration. The Abl family have significant structural homology to the Src tyrosine kinase family, but have a unique long carboxy-terminal extension that contains protein-protein interaction sites and acts as the binding site for targets such as ATM, p53 and pRb. c-Abl is medically important as there is a causal link between the Abl-Bcr fusion protein (caused by a t(9,22) translocation) and development of chronic myeloid leukemia.