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The calcineurin pathway links hyperpolarization (Kir2.1)-induced Ca2+ signals to human myoblast differentiation and fusion

Beguet, Anne
Published in Development. 2006, vol. 133, no. 16, p. 3107-3114
Abstract In human myoblasts triggered to differentiate, a hyperpolarization, resulting from K+ channel (Kir2.1) activation, allows the generation of an intracellular Ca2+ signal. This signal induces an increase in expression/activity of two key transcription factors of the differentiation process, myogenin and MEF2. Blocking hyperpolarization inhibits myoblast differentiation. The link between hyperpolarization-induced Ca2+ signals and the four main regulatory pathways involved in myoblast differentiation was the object of this study. Of the calcineurin, p38-MAPK, PI3K and CaMK pathways, only the calcineurin pathway was inhibited when Kir2.1-linked hyperpolarization was blocked. The CaMK pathway, although Ca2+ dependent, is unaffected by changes in membrane potential or block of Kir2.1 channels. Concerning the p38-MAPK and PI3K pathways, their activity is present already in proliferating myoblasts and they are unaffected by hyperpolarization or Kir2.1 channel block. We conclude that the Kir2.1-induced hyperpolarization triggers human myoblast differentiation via the activation of the calcineurin pathway, which, in turn, induces expression/activity of myogenin and MEF2.
Keywords Calcineurin/ metabolismCalcium SignalingCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium-Calmodulin-Dependent Protein Kinases/metabolismCell DifferentiationCell FusionCell Membrane/metabolismCell PolarityHumansMyoblasts/ cytology/metabolismMyogenic Regulatory Factors/metabolismMyogenin/metabolismPotassium Channels, Inwardly Rectifying/ metabolismP38 Mitogen-Activated Protein Kinases/metabolism
PMID: 16831831
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Other version: http://dev.biologists.org/content/133/16/3107.full.pdf
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KONIG, Stéphane et al. The calcineurin pathway links hyperpolarization (Kir2.1)-induced Ca2+ signals to human myoblast differentiation and fusion. In: Development, 2006, vol. 133, n° 16, p. 3107-3114. doi: 10.1242/dev.02479 https://archive-ouverte.unige.ch/unige:10323

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Deposited on : 2010-08-06

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