ABL1

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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FISH analysis for the BCR and ABL1 regions can detect almost all variants of this rearrangement.
IS] or undetectable disease in complimentary DNA(cDNA) with [greater than or equal to] 10000 ABL1 transcripts], and MR [4, 5] (detectable disease [less than or equal to] 0.
The tyrosine kinase ABL1 becomes fused to the BCR protein as a result of a balanced chromosome translocation, t(9;22), in individuals with CML.
Exposing these cancer cells to amounts of noradrenaline similar to those found in ovarian tissues both under normal and stressed conditions showed that the noradrenaline levels during stress activated Src pathways that in turn caused a cascade of kinase pathways to be activated, including KIT, EGFR, ABL1, and IGF-1.
50] values ranging from 1 to 10 [micro]M, and was also an effective inhibitor of several important kinases such as ABL1, CDK4, CHK1, PKC, c-MET, FGFR, and others (Villalonga et al.
control of the cell 2006 cycle at the G1/S (start) transition 11 ABL1 Regulates cytoskeleton Chiaretti et al.
CACNA1D, EDNRA, KCNG2, NR3C2, PDE4D, ACE, ADRA1B, ADRB3, KCNJ11, ADRAJD Cardiac dilation Imipramine EPO, NOS1 Pulmonary hypertension EtOH-Fr EDNRB, FTGER3, PDE5A Pulmonary hypertension Imipramine EPO, EDNRB, FLT3, ABL1, EDNRA, ADRA1B, ADRB3, ADRA1D Increased levels of alkaline EtOH-Fr VEGFA phosphatase Bold indicate that these genes are prevalent in several disease clusters.
2), with generation of the BCRABL1 fusion gene and constitutive activation of the ABL1 kinase, which is the underlying molecular mechanism for the development of CML and the basis for targeted therapy with small-molecule tyrosine kinase inhibitors, such as imatinib.
To generate a reproducible and lasting source of reference material, synthetic and nuclease-resistant ABL1, BCR, and BCR-ABL1 transcripts were prepared on a large scale with the validated ARQ manufacturing process (see Figs.
2) (known as Ph), resulting in the presence of BCR-ABL1 mRNA transcripts and an abnormal fusion protein with constitutive ABL1 tyrosine kinase activity.
Standard quantitative analyses of BCR-ABL [fusion gene of BCR [5] (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and the total number of ABL transcripts were performed as previously described (17).