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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
