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• W2000481753 abstract "The kinase Mirk/dyrk1B is essential for the differentiation of C2C12myoblasts. Mirk reinforces the G₀/G₁ arrest state inwhich differentiation occurs by directly phosphorylating and stabilizingp27^Kip1 and destabilizing cyclin D1. We now demonstrate that Mirkis anti-apoptotic in myoblasts. Knockdown of endogenous Mirk by RNAinterference activated caspase 3 and decreased myoblast survival by 75%,whereas transient overexpression of Mirk increased cell survival. Mirk exertsits anti-apoptotic effects during muscle differentiation at least in partthrough effects on the cell cycle inhibitor and pro-survival moleculep21^Cip1. Overexpression and RNA interference experimentsdemonstrated that Mirk phosphorylates p21 within its nuclear localizationdomain at Ser-153 causing a portion of the typically nuclear p21 to localizein the cytoplasm. Phosphomimetic GFP-p21-S153D was pancellular in both cyclingC2C12 myoblasts and NIH3T3 cells. Endogenous Mirk in myotubes andoverexpressed Mirk in NIH3T3 cells were able to cause the pancellularlocalization of wild-type GFP-p21 but not the nonphosphorylatable mutantGFP-p21-S153A. Translocation to the cytoplasm enables p21 to block apoptosisthrough inhibitory interaction with pro-apoptotic molecules. Phosphomimeticp21-S153D was more effective than wild-type p21 in blocking the activation ofcaspase 3. Transient expression of p21-S153D also increased myoblast viabilityin colony forming assays, whereas the p21-S153A mutant had no effect. ThisMirk-dependent change in p21 intracellular localization is a natural part ofmyoblast differentiation. Endogenous p21 localized exclusively to the nucleiof proliferating myoblasts but was also found in the cytoplasm of post-mitoticmultinucleated myotubes and adult human skeletal myofibers." @default.
• W2000481753 created "2016-06-24" @default.
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• W2000481753 date "2005-07-01" @default.
• W2000481753 modified "2023-10-14" @default.
• W2000481753 title "Mirk/Dyrk1B Mediates Survival during the Differentiation of C2C12Myoblasts" @default.
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• W2000481753 doi "https://doi.org/10.1074/jbc.m413594200" @default.
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