biostudies-literatureSun QANHLBI NIH HHSNational Institutes of HealthNational Heart Lung and Blood Institute150163https://www.ebi.ac.uk/biostudies/studies/S-EPMC12651786biostudies-literatureUnknown723Excitation-contraction coupling in skeletal muscle myofibers depends upon Ca²⁺ release from the sarcoplasmic reticulum through the ryanodine receptor/Ca²⁺-release channel RyR1. The RyR1 contains ∼100 Cys thiols of which ∼30 comprise an allosteric network subject to posttranslational modification by S-nitrosylation, S-palmitoylation and S-oxidation. However, the role and function of these modifications is not understood. Although aberrant S-nitrosylation of multiple unidentified sites has been associated with dystrophic diseases, malignant hyperthermia and other myopathic syndromes, S-nitrosylation in physiological situations is reportedly specific to a single (1 of ∼100) Cys in RyR1, Cys³⁶³⁶ in a manner gated by pO₂. Using mice expressing a form Biochemical and biophysical research communicationsPhysiological role for S-nitrosylation of RyR1 in skeletal muscle function and development.PMC12651786R01 HL059130RO1 HL0591130Hess DTPlummer BNPremont RTSun QAQian ZLaurita KRChaube RStamler JSVenetos NMGrimmett ZWPerez LGfalsePhysiological role for S-nitrosylation of RyR1 in skeletal muscle function and development.Excitation-contraction coupling in skeletal muscle myofibers depends upon Ca²⁺ release from the sarcoplasmic reticulum through the ryanodine receptor/Ca²⁺-release channel RyR1. The RyR1 contains ∼100 Cys thiols of which ∼30 comprise an allosteric network subject to posttranslational modification by S-nitrosylation, S-palmitoylation and S-oxidation. However, the role and function of these modifications is not understood. Although aberrant S-nitrosylation of multiple unidentified sites has been associated with dystrophic diseases, malignant hyperthermia and other myopathic syndromes, S-nitrosylation in physiological situations is reportedly specific to a single (1 of ∼100) Cys in RyR1, Cys³⁶³⁶ in a manner gated by pO₂. Using mice expressing a form 2024-01-01T00:00:00Z2024 Sep2026-06-05T18:44:55.433Z2026-05-20T03:13:12.73ZS-EPMC126517863882062610.1016/j.bbrc.2024.150163