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Ryanodine receptor luminal Ca2+ regulation: swapping calsequestrin and channel isoforms. | LitMetric

AI Article Synopsis

  • The sarcoplasmic reticulum (SR) in striated muscle releases calcium (Ca(2+)) through a protein complex involving the ryanodine receptor (RyR) channel and the protein calsequestrin (CSQ), which also helps buffer calcium.
  • The research investigates how CSQ affects the function of skeletal (RyR1) and cardiac (RyR2) calcium channels by adding different CSQ proteins to see how they influence calcium sensitivity.
  • Findings show that while CSQ enhances the calcium sensitivity of RyR2 channels significantly, it has little to no effect on RyR1 channels, suggesting CSQ mainly serves as a calcium buffer in skeletal muscle rather

Article Abstract

Sarcoplasmic reticulum (SR) Ca(2+) release in striated muscle is mediated by a multiprotein complex that includes the ryanodine receptor (RyR) Ca(2+) channel and the intra-SR Ca(2+) buffering protein calsequestrin (CSQ). Besides its buffering role, CSQ is thought to regulate RyR channel function. Here, CSQ-dependent luminal Ca(2+) regulation of skeletal (RyR1) and cardiac (RyR2) channels is explored. Skeletal (CSQ1) or cardiac (CSQ2) calsequestrin were systematically added to the luminal side of single RyR1 or RyR2 channels. The luminal Ca(2+) dependence of open probability (Po) over the physiologically relevant range (0.05-1 mM Ca(2+)) was defined for each of the four RyR/CSQ isoform pairings. We found that the luminal Ca(2+) sensitivity of single RyR2 channels was substantial when either CSQ isoform was present. In contrast, no significant luminal Ca(2+) sensitivity of single RyR1 channels was detected in the presence of either CSQ isoform. We conclude that CSQ-dependent luminal Ca(2+) regulation of single RyR2 channels lacks CSQ isoform specificity, and that CSQ-dependent luminal Ca(2+) regulation in skeletal muscle likely plays a relatively minor (if any) role in regulating the RyR1 channel activity, indicating that the chief role of CSQ1 in this tissue is as an intra-SR Ca(2+) buffer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756356PMC
http://dx.doi.org/10.1016/j.bpj.2009.07.030DOI Listing

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