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• W2004966843 startingPage "1147" @default.
• W2004966843 abstract "Activation of the transcription factor FKHR (Forkhead in human rhabdomyosarcoma, FOXO1a) in various established cell lines induces cell cycle arrest followed by apoptosis. These effects are inhibited through activation of the phosphatidylinositol 3-kinase/Akt pathway, resulting in FKHR phosphorylation and its export from the nucleus, thus blocking its pro-apoptotic activity. Here we report that FKHR regulates fusion of differentiating primary myoblasts. We demonstrate that FKHR is localized in the cytoplasm of proliferating myoblasts, yet translocates to the nucleus by a phosphorylation-independent pathway following serum starvation, a condition that induces myoblast differentiation. FKHR phosphorylation during terminal differentiation appears to downregulate its fusion activity, as a dominant-active non-phosphorylatable FKHR mutant dramatically augments the rate and extent of myotube fusion. However, this FKHR mutant exerts its effects only after other events initiated the differentiation pro cess. Conversely, enforced expression of a dominant-negative FKHR mutant blocks myotube formation whereas wild-type FKHR has no effect. We conclude that in addition to the role of FoxO proteins in regulating cell cycle progress and apoptosis, FKHR controls the rate of myotube fusion during myogenic differentiation." @default.
• W2004966843 created "2016-06-24" @default.
• W2004966843 creator A5013801580 @default.
• W2004966843 creator A5026036897 @default.
• W2004966843 date "2003-03-03" @default.
• W2004966843 modified "2023-10-18" @default.
• W2004966843 title "FKHR (FOXO1a) is required for myotube fusion of primary mouse myoblasts" @default.
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• W2004966843 doi "https://doi.org/10.1093/emboj/cdg116" @default.
• W2004966843 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/150349" @default.
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