Calsequestrin depolymerization acts as a channel closing switch to limit calcium depletion and prevent catastrophic structural changes in the sarcoplasmic reticulum.
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Calsequestrin may safeguard SR integrity during calcium release in animal models; leaves open clinical translation to human arrhythmias.
] went down: fully when calcium depletion was maximal (a condition achieved with an SR calcium channel opening drug) and partially when depletion was limited (a condition imposed by fatiguing stimulation, long-lasting depolarization, or low drug concentrations). With fluorescence and electron microscopic imaging we demonstrated massive movements of calsequestrin accompanied by drastic morphological SR changes in fully depleted cells. When cells were partially depleted no remodeling was found. The present results support the proposed role of calsequestrin in termination of calcium release by conformationally inducing closure of SR channels. A channel closing switch operated by calsequestrin depolymerization will limit depletion, thereby preventing full disassembly of the polymeric calsequestrin network and catastrophic structural changes in the SR.
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Manno et al. (2017) studied this question.
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