Pre-assembled Ca2+ entry units and constitutively active Ca2+ entry in skeletal muscle of calsequestrin-1 knockout mice.

摘要: Store-operated Ca2+ entry (SOCE) is a ubiquitous influx mechanism triggered by depletion of stores from the endoplasmic/sarcoplasmic reticulum (ER/SR). We recently reported that acute exercise in WT mice drives formation units (CEUs), intracellular junctions contain STIM1 and Orai1, two key proteins mediating SOCE. The presence CEUs correlates with increased constitutive- store-operated entry, as well sustained release force generation during repetitive stimulation. Skeletal muscle lacking calsequestrin-1 (CASQ1-null), primary Ca2+-binding protein lumen SR terminal cisternae, exhibits significantly reduced total store content marked high-frequency Here, we report are constitutively assembled extensor digitorum longus (EDL) flexor brevis (FDB) muscles sedentary CASQ1-null mice. higher density EDL (39.6 ± 2.1/100 µm2 versus 2.0 0.3/100 µm2) FDB (16.7 1.0/100 2.7 0.5/100 compared correlated enhanced expression STIM1, SERCA. ability to recover ions via SOCE served promote maintenance peak transient amplitude, dependence luminal replenishment on BTP-2-sensitive SOCE, contractile repetitive, Together, these data suggest compensate for lack CASQ1 reduction releasable assembling constitutive entry.