ABL1

(redirected from c-ABL)

ABL1

A gene on chromosome 9q34.1 that encodes a cytoplasmic and nuclear protein tyrosine kinase involved in cell differentiation, cell division, cell adhesion and stress response. ABL1 is negatively regulated by its SH3 domain.

Molecular pathology
Deletion of the SH3 domain turns ABL1 into an oncogene; the t(9;22) translocation results in the head-to-tail fusion of BCR and ABL1, which is present in many cases of CML.
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M2 PHARMA-October 26, 2017-1ST Bio partners with Neuraly to advance novel c-Abl Inhibitors for Parkinson's Disease
M2 EQUITYBITES-October 26, 2017-1ST Bio partners with Neuraly to advance novel c-Abl Inhibitors for Parkinson's Disease
In cytoplasm, Prdx1 exists as a protein complex with c-Abl-SH domain and protects c-Abl from phosphorylation.
Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD1 73955 and imatinib (STI-571).
Molecular studies revealed this involved the c-ABL gene on chromosome 9 and the BCR gene on chromosome 22, producing a fusion gene on the derivative chromosome 22 of the 5' region of BCR with the 3' region of the c-ABL gene.
6] Human genes: KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; HER2, human epidermal growth factor receptor 2; current symbol and name: ERBB2, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/ glioblastoma derived oncogene homolog (avian); BRAF, v-raf murine sarcoma viral oncogene homolog B1; BCR, breakpoint cluster region; ABL, c-abl oncogene 1, non-receptor tyrosine kinase; ALK, anaplastic lymphoma receptor tyrosine kinase.
Summary: TEHRAN (FNA)- After decades of studying the pathological process that wipes out large volumes of memory, scientists discovered a molecule called c-Abl that has a known role in leukemia also has a hand in Alzheimer's disease.
Washington, May 25 (ANI): The Feinstein Institute for Medical Research scientists have discovered that a molecule c-Abl, which has a known role in leukaemia, also has a hand in Alzheimer's disease.
The c-abl proto-oncogene is translocated from chromosome 9 to the breakpoint cluster region on chromosome 22.
The remarkable success of Gleevec(TM) in treating chronic myelogenous leukemia is based on inhibition of the c-Abl kinase, whose activity, like c-Kit's, is tightly controlled in normal cells.
C-Abl contributes to the regulation of cell death and is implicated in a host of diseases.
5] Human genes: BCR, breakpoint cluster region; ABL1, c-abl oncogene 1, receptor tyrosine kinase; GUSB, glucuronidase, beta.