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

2 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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Ryanodine Receptor Calcium Release Channel
Post Translational Protein Processing
Muscle
Myocardium
Skeletal Muscle
Sarcoplasmic Reticulum
Oxidation-Reduction
Macromolecular Substances
Excitation Contraction Coupling
Extracellular Space
Muscular Diseases
Phosphors
Cytoplasm
Heart Failure
Ions
Calcium
Muscles
Proteins

Cite this

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title = "Ryanodine receptor Ca 2+ release channel post-translational modification: Central player in cardiac and skeletal muscle disease",
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.",
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T1 - Ryanodine receptor Ca 2+ release channel post-translational modification

T2 - Central player in cardiac and skeletal muscle disease

AU - Denniss, Amanda

AU - Dulhunty, Angela F.

AU - Beard, Nicole A.

PY - 2018/8/1

Y1 - 2018/8/1

N2 - 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.

AB - 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.

KW - Myopathy

KW - Phosphorylation

KW - Reactive oxygen species

KW - Ryanodine receptor

KW - Reactive Oxygen Species/metabolism

KW - Ryanodine Receptor Calcium Release Channel/genetics

KW - Heart Failure/genetics

KW - Humans

KW - Sarcoplasmic Reticulum/metabolism

KW - Muscle, Skeletal/metabolism

KW - Myotonia Congenita/genetics

KW - Calcium/metabolism

KW - Animals

KW - Myocardium/metabolism

KW - Excitation Contraction Coupling/physiology

KW - Protein Processing, Post-Translational

KW - Muscle Contraction/physiology

KW - Calcium Signaling

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UR - http://www.mendeley.com/research/ryanodine-receptor-ca-2-release-channel-posttranslational-modification-central-player-cardiac-skelet

U2 - 10.1016/j.biocel.2018.05.004

DO - 10.1016/j.biocel.2018.05.004

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EP - 53

JO - International Journal of Biochemistry and Cell Biology

JF - International Journal of Biochemistry and Cell Biology

SN - 1357-2725

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