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Modulation of ryanodine receptor by luminal calcium and accessory proteins in health and cardiac disease Gyorke S; Terentyev DCardiovasc Res 2008[Jan]; 77 (2): 245-55The cardiac ryanodine receptor (RyR2) is the sarcoplasmic reticulum (SR) Ca(2+) release channel which is responsible for generation of the cytosolic Ca(2+) transient required for activation of cardiac contraction. RyR2 functional activity is governed by changes in [Ca(2+)] on both the cytosolic and luminal phase of the RyR2 channel. Activation of RyR2 by cytosolic Ca(2+) results in Ca(2+)-induced Ca(2+) release (CICR) from the SR. The decline in luminal [Ca(2+)] following release contributes to termination of CICR and Ca(2+) signalling refractoriness through the process of luminal Ca(2+)-dependent deactivation of RyR2s. The control of RyR2s by luminal Ca(2+) involves coordinated interaction of the channel with several SR proteins, including the Ca(2+)-binding protein calsequestrin (CASQ2), and the integral proteins triadin 1 (TRD) and junctin (JCN). CASQ2 in addition to serving as a Ca(2+) storage site and a luminal Ca(2+) buffer modulates RyR2 function more directly as a putative luminal Ca(2+) sensor. TRD and JCN, stimulatory by themselves, mediate the interactions between CASQ2 and RyR2. Acquired and genetic defects in proteins of this junctional Ca(2+) signalling complex lead to disease states such as cardiac arrhythmia and heart failure by impairing luminal Ca(2+) regulation of RyR2.|Animals[MESH]|Arrhythmias, Cardiac/etiology[MESH]|Calcium Signaling[MESH]|Calcium-Binding Proteins/*physiology[MESH]|Calcium/*physiology[MESH]|Calsequestrin/genetics/*physiology[MESH]|Carrier Proteins/*physiology[MESH]|Heart Diseases/*etiology/metabolism[MESH]|Heart Failure/etiology[MESH]|Humans[MESH]|Membrane Proteins/*physiology[MESH]|Mixed Function Oxygenases/*physiology[MESH]|Muscle Proteins/*physiology[MESH]|Polymorphism, Genetic[MESH]|Ryanodine Receptor Calcium Release Channel/chemistry/*physiology[MESH]|Sarcoplasmic Reticulum/metabolism[MESH] |
