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Figure 5


Fig. 5. Schematic representation of the role of membrane hyperpolarization during human myoblast differentiation. Chronological illustration of the mechanisms of myoblast differentiation, that begins with calcineurin activation as a consequence of Kir2.1-induced membrane hyperpolarization. Calcineurin activation is strictly associated with Kir2.1 activity and the onset of the differentiation process. Activation of Ca2+ influx through T-type Ca2+ channels (CaT) or store-operated channels (SOCs), or release of Ca2+ for endoplasmic reticulum (stores), could provide the increase of intracellular Ca2+ concentration responsible for myoblast differentiation and calcineurin activation (Arnaudeau et al., 2006). However, p38-MAPK, PI3K and CaMK are (or can be) activated during myoblast proliferation without inducing myoblast differentiation. CaMK can be activated by an increase in extracellular Ca2+ concentration not linked to the differentiation process. Myogenin and MEF2 expression is observed after calcineurin activation.





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