作者: Barbara Mosca , Jan Eckhardt , Leda Bergamelli , Susan Treves , Rossana Bongianino
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摘要: We exploited a variety of mouse models to assess the roles JP45-CASQ1 (CASQ, calsequestrin) and JP45-CASQ2 on calcium entry in slow twitch muscles. In flexor digitorum brevis (FDB) fibers isolated from JP45-CASQ1-CASQ2 triple KO mice, transients induced by tetanic stimulation rely via La3+- nifedipine-sensitive channels. The comparison excitation-coupled (ECCE) between FDB WT, JP45KO, CASQ1KO, CASQ2KO, double KO, shows that ECCE enhancement requires ablation both CASQs JP45. Calcium activated complexes supports force development soleus addition, we show interact with JP45 at Ca2+ concentrations similar those present lumen sarcoplasmic reticulum rest, whereas SR after depolarization-induced release cause dissociation CASQs. Our results complex JP45-CASQs is negative regulator muscles supported dynamic interaction