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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)....
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| Udgivet i: | Physiol Rep |
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| Main Authors: | , , , , , , , |
| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
John Wiley and Sons Inc.
2018
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| Fag: | |
| Online adgang: | 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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