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• W2019960565 abstract "ABL gene translocations create constitutively active tyrosine kinases that are causative in chronic myeloid leukemia, acute lymphocytic leukemia and other hematopoietic malignancies. Consistent retention of ABL SH3/SH2 autoinhibitory domains, however, suggests that these leukemogenic tyrosine kinase fusion proteins remain subject to regulation. We resolve this paradox, demonstrating that BCR-ABL1 kinase activity is regulated by RIN1, an ABL SH3/SH2 binding protein. BCR-ABL1 activity was increased by RIN1 overexpression and decreased by RIN1 silencing. Moreover, Rin1−/− bone marrow cells were not transformed by BCR-ABL1, ETV6-ABL1 or BCR-ABL1T315I, a patient-derived drug-resistant mutant, as judged by growth factor independence. Rescue by ectopic RIN1 verified a cell autonomous mechanism of collaboration with BCR-ABL1 during transformation. Sensitivity to the ABL kinase inhibitor imatinib was increased by RIN1 silencing, consistent with RIN1 stabilization of an activated BCR-ABL1 conformation having reduced drug affinity. The dependence on activation by RIN1 to unleash full catalytic and cell transformation potential reveals a previously unknown vulnerability that could be exploited for treatment of leukemic cases driven by ABL translocations. The findings suggest that RIN1 targeting could be efficacious for imatinib-resistant disease and might complement ABL kinase inhibitors in first-line therapy." @default.
• W2019960565 created "2016-06-24" @default.
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• W2019960565 date "2010-11-19" @default.
• W2019960565 modified "2023-10-13" @default.
• W2019960565 title "ABL fusion oncogene transformation and inhibitor sensitivity are mediated by the cellular regulator RIN1" @default.
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• W2019960565 doi "https://doi.org/10.1038/leu.2010.268" @default.
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