Abstract
In this issue, Michelucci et al. report the existence of specific sites acting as Ca(2+) entry units (CEUs) in fast skeletal muscle of mice lacking calsequestrin (CASQ1), the major Ca(2+) binding protein of the SR. The CEU provides constitutive and store-operated Ca(2+) entry (SOCE) and resistance to force decline resulting from SR Ca(2+) depletion during repetitive muscle activity.