Ryanodine receptor Ca 2+ release channel post-translational modification

Central player in cardiac and skeletal muscle disease

Amanda Denniss, Angela F. Dulhunty, Nicole A. Beard

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Calcium release from internal stores is a quintessential event in excitation-contraction coupling in cardiac and skeletal muscle. The ryanodine receptor Ca 2+ release channel is embedded in the internal sarcoplasmic reticulum Ca 2+ store, which releases Ca 2+ into the cytoplasm, enabling contraction. Ryanodine receptors form the hub of a macromolecular complex extending from the extracellular space to the sarcoplasmic reticulum lumen. Ryanodine receptor activity is influenced by the integrated effects of associated co-proteins, ions, and post-translational phosphor and redox modifications. In healthy muscle, ryanodine receptors are phosphorylated and redox modified to basal levels, to support cellular function. A pathological increase in the degree of both post-translational modifications disturbs intracellular Ca 2+ signalling, and is implicated in various cardiac and skeletal disorders. This review summarises our current understanding of the mechanisms linking ryanodine receptor post-translational modification to heart failure and skeletal myopathy and highlights the challenges and controversies within the field.

Original languageEnglish
Pages (from-to)49-53
Number of pages5
JournalInternational Journal of Biochemistry and Cell Biology
Volume101
DOIs
Publication statusPublished - 1 Aug 2018

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