Loss of S100A1 expression leads to Ca(2+) release potentiation in mutant mice with disrupted CaM and S100A1 binding to CaMBD2 of RyR1

Calmodulin (CaM) and S100A1 fine‐tune skeletal muscle Ca(2+) release via opposite modulation of the ryanodine receptor type 1 (RyR1). Binding to and modulation of RyR1 by CaM and S100A1 occurs predominantly at the region ranging from amino acid residue 3614‐3640 of RyR1 (here referred to as CaMBD2)....

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Publicado en:Physiol Rep
Autores principales: Hernández‐Ochoa, Erick O., Melville, Zephan, Vanegas, Camilo, Varney, Kristen M., Wilder, Paul T., Melzer, Werner, Weber, David J., Schneider, Martin F.
Formato: Artigo
Lenguaje:Inglês
Publicado: John Wiley and Sons Inc. 2018
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Original Research
Acceso en línea:https://ncbi.nlm.nih.gov/pmc/articles/PMC6087734/
https://ncbi.nlm.nih.gov/pubmed/30101473
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.14814/phy2.13822
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