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- W2101471927 startingPage "3533" @default.
- W2101471927 abstract "Glycogen synthase kinase 3β (GSK3β) regulates diverse physiological processes, including metabolism, development, oncogenesis, and neuroprotection. GSK3β kinase activity has been reported to be critical for various types of cancer cells, but the mechanism has remained elusive. In this study we examine the mechanism by which GSK3β regulates the survival of leukemia cells. We demonstrate that upon GSK3β kinase inhibition different types of leukemia cells show severe proliferation defects as a result of apoptosis. The transcription factor c-Myb is found to be the main target of GSK3β inhibition in cell survival. GSK3β inactivation reduces the expression of c-Myb by promoting its ubiquitination-mediated degradation, thereby inhibiting the expression of c-Myb–dependent antiapoptotic genes Bcl2 and survivin. Coimmunoprecipitation, reporter assays, chromatin immunoprecipitation, and knockdown studies show that c-Myb needs to interact and cooperate with transcription factor LEF-1 in the activation of Bcl2 and survivin and that both transcription factors are required for cell survival. These data reveal an as-yet-unknown mechanism by which GSK3β controls cell survival." @default.
- W2101471927 created "2016-06-24" @default.
- W2101471927 creator A5012163087 @default.
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- W2101471927 creator A5046914597 @default.
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- W2101471927 date "2011-09-15" @default.
- W2101471927 modified "2023-09-27" @default.
- W2101471927 title "GSK3β inactivation induces apoptosis of leukemia cells by repressing the function of c-Myb" @default.
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- W2101471927 doi "https://doi.org/10.1091/mbc.e11-06-0483" @default.
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- W2101471927 hasPublicationYear "2011" @default.
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