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• W3199808150 abstract "Glycogen synthase kinase 3 (GSK3) is a ubiquitously expressed kinase involved in a myriad of biological processes. Although GSK3 mediated phosphorylation has been shown to induce the degradation of many pro-survival and pro-proliferation factors, cancer cells of different origin show reduced proliferation or survival after GSK3 inhibition. Our current understanding of the role GSK3 plays in normal mature B cells, B cell precursors and transformed B cells is incomplete and does not allow to assess whether GSK3 inhibitors can be used to treat B cell derived malignancies. Here we identify β-catenin as the major factor driving GSK3-inhibition induced changes in B cells. We show that β-catenin accumulation has opposing effects on cell metabolism and survival in mature B cells and B cell precursors. Moreover, we demonstrate that β-catenin destabilizes the commitment to the B cell lineage. In summary, our study identifies β-catenin induced signaling as a factor that can be exploited to limit the survival of malignant B cells." @default.
• W3199808150 created "2021-09-27" @default.
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• W3199808150 date "2021-09-18" @default.
• W3199808150 modified "2023-09-27" @default.
• W3199808150 title "Accumulation of the GSK3 target protein β-catenin is lethal for B cell precursors and malignant B cells" @default.
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• W3199808150 doi "https://doi.org/10.1101/2021.09.17.460779" @default.
• W3199808150 hasPublicationYear "2021" @default.
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