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Figure 9


Fig. 9. Hypothetical model for enhanced store-operated Ca2+ entry in dystrophic skeletal muscle fibers. In skeletal muscle, ryanodine receptors (RyR) are allosterically activated by L-type voltage-gated Ca2+ channels (VGCC) when plasma membrane (PM) is depolarized ({Delta}V). SR Ca2+ released through ryanodine receptors triggers contraction and Ca2+ is pumped back into the SR by the SERCA. Ca2+-store depletion occurring during Ca2+ release through ryanodine receptors or when SERCA is blocked by thapsigargin triggers iPLA2 activation, possibly by the release of calcium influx factor (CIF). Hydrolysis products of iPLA2 (most likely lysophospholipids) may be responsible for SOC stimulation and Ca2+ influx. Overexpression of iPLA2 in dystrophic muscle is likely to be responsible for enhanced Ca2+ influx through SOC.





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