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- W1524403169 abstract "2782 The BCR-ABL oncoprotein of Chronic Myelogenous Leukemia (CML) localizes to the cell cytoplasm because its nuclear localization signals (NLS) are inactivated. In the cytoplasm, BCR-ABL activates several proliferative and anti-apoptotic signaling pathways leading to the development of CML. We have previously reported that the NLS of BCR-ABL can be re-activated and that the nuclear BCR-ABL can trigger cell death. To clarify the molecular mechanisms responsible for the apoptosis induced by nuclear BCR-ABL, we investigated its possible interactions with the p53 family of proteins. We engineered a BCR-ABLNuk construct that is capable of nuclear import while maintaining its constitutive tyrosine kinase activity. Immunofluorescence analysis and cell fractionation experiments confirmed that BCR-ABLNuk and its kinase defective counterpart BCR-ABLKDNuk both migrate to the cell nucleus. Furthermore, IP-Western experiments demonstrated that these constructs physically interact with p73 but not with p53 and p63. This interaction requires the SH3 domain of BCR-ABLNuk, since a BCR-ABLNuk construct devoid of the SH3 domain can no longer bind p73. Following its association with BCR-ABLNuk, p73 is phosphorylated on tyrosines 99 and 121. This post-translational modification stabilizes the p73 protein and leads to the induction of cell death. These results were further confirmed in fibroblasts derived from p73-null mice. In this cellular context, BCR-ABLNuk was unable to elicit cell death. However, the reconstitution of these cells with wild-type p73 promptly reestablished an apoptotic response. Our results identify p73 as a molecular target of nuclear BCR-ABL, suggesting that, in order to induce cell death, the oncoprotein requires binding and phosphorylation of p73." @default.
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- W1524403169 date "2008-05-01" @default.
- W1524403169 modified "2023-09-23" @default.
- W1524403169 title "p73 is required for the apoptotic activity of an engineered nuclear BCR-ABL tyrosine kinase" @default.
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