Oncogenic E17K mutation in the pleckstrin homology domain of AKT1 promotes v-Abl-mediated pre-B-cell transformation and survival of Pim-deficient cells.
作者： G Guo , X Qiu , S Wang , Y Chen , P B Rothman
DOI: 10.1038/ONC.2010.149
关键词:
摘要: Abl-mediated transformation requires the activation of multiple pathways involved in cellular proliferation and survival, including PI3K/AKT JAK/STAT-dependent Pim kinases. Recently, E17K mutation AKT1 has been associated with human malignancies leukemia mice. However, this not identified Abl-transformed cells. We investigated presence AKT1(E17K) v-Abl-transformed cell clones. was detected 3 (2.6%) 116 specimens examined. To show involvement directly v-Abl-mediated tumorigenesis, we infected bone marrow cells from mice bicistronic retroviruses encoding v-Abl either wild-type or mutant AKT1. Interestingly, found that greatly increased efficiency as compared Ectopic expression levels antiapoptotic protein BCL2 phosphorylation proapoptotic BAD. This correlated an protection imatinib-induced apoptosis Abl transformants. Furthermore, promotes survival Pim-deficient cells, indicating a functional link between AKT transformation. In addition, delays loss Pim-1 Pim-2 on inactivation, which suggests there exists reciprocal signaling
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