Mitsugumin 53 regulates extracellular Ca2+ entry and intracellular Ca2+ release via Orai1 and RyR1 in skeletal muscle

• DOI: 10.1038/srep36909
• Publication Date: 2016-11-14T10:25:48Z
• Authors: Mi Kyoung Ahn; Keon Jin Lee; Chuanxi Cai; Mei Huang; Chung-Hyun Cho; Jianjie Ma; Eun Hui Lee
• Keywords: Orai1

Mitsugumin 53 (MG53) participates in the membrane repair of various cells, and skeletal muscle is major tissue that expresses MG53. Except for regulatory effects MG53 on SERCA1a, role(s) unique functions such as contraction have not been well examined. Here, a new MG53-interacting protein, Orai1, identified muscle. To examine functional relevance MG53-Orai1 interaction, was over-expressed mouse primary or C2C12 myotubes properties were examined using cell physiological biochemical approaches. The PRY-SPRY region binds to Orai1 are co-localized plasma myotubes. interaction enhances extracellular Ca2+ entry via store-operated (SOCE) mechanism Interestingly, over-expressing display reduced intracellular release response K+-membrane depolarization caffeine stimulation, suggesting reduction RyR1 channel activity. Expressions TRPC3, TRPC4, calmodulin 1 increased myotubes, directly which suggests possibility TRPC3 also enhanced entry. Thus, could participate regulating during SOCE contraction.