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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)....
| Autores principales: | , , , , , , , |
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
| Publicado: |
John Wiley and Sons Inc.
2018
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087734/ https://www.ncbi.nlm.nih.gov/pubmed/30101473 http://dx.doi.org/10.14814/phy2.13822 |