Abstract
Calcium (Ca2+) is a key mediator in a wide range of cellular functions. Ca2+ released from the sarcoplasmic reticulum (SR) induces sarcomeric contraction of myofibrils, which is a primary mechanism mediating Ca2+ homeostasis in skeletal muscle. At the depletion of Ca2+ in the SR, store-operated Ca2+ entry (SOCE) is induced to obtain Ca2+ from the extracellular area. SR protein, STIM1 and Ca2+ channel protein on the plasma membrane, ORAI1 work on SOCE in skeletal myofibers. Tubular aggregate myopathy (TAM) has been known to be caused by constitutively activated SOCE owing to the dominant mutations in ORAI1 or STIM1 consequently.
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