Rem inhibits skeletal muscle EC coupling by reducing the number of functional L-type Ca2+ channels.

摘要: Abstract In skeletal muscle, the L-type voltage-gated Ca 2+ channel (1,4-dihydropyridine receptor) serves as voltage sensor for excitation-contraction (EC) coupling. this study, we examined effects of Rem, a member RGK \( R _ em , 2 ad / ir \) family Ras-related monomeric GTP-binding proteins, on function muscle channel. EC coupling was found to be weakened in myotubes expressing Rem tagged with enhanced yellow fluorescent protein (YFP-Rem), assayed by electrically evoked contractions and myoplasmic transients. This impaired not consequence altered type 1 ryanodine receptor, or reduced stores, since application 4-chloro- m -cresol, direct receptor activator, elicited release YFP-Rem-expressing that distinguishable from control myotubes. However, YFP-Rem magnitude current ∼75% produced concomitant reduction membrane-bound charge movements. Thus, our results indicate negatively regulates reducing number functional channels plasma membrane.