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Dysregulation of the Gain of CICR Through Ryanodine Receptor1 (RyR1): The Putative Mechanism Underlying Malignant Hyperthermia

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Regulatory Mechanisms of Striated Muscle Contraction

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 592))

Abstract

Ca2+ released through the Ca2+ release channel triggers muscle contraction. The Ca2+ release channel in the sarcoplasmic reticulum (SR) of the striated muscles is referred to as the ryanodine receptor (RyR), and is so named because of its binding ability of the open state with a high affinity to ryanodine.16 Three genetically distinct isoforms (RyR1-3) are identified in mammals: RyR1 is the primary isoform in the skeletal muscle, RyR2 in the cardiac muscle, and RyR3 is ubiquitously expressed, although in a minuscule amount. In non-mammalian vertebrate skeletal muscles, e.g., chicken, frog, and fish, two isoforms referred to as α- and β-RyR are expressed in almost equal amounts. Further studies show that α- and β-RyR are homologs of RyR1 and RyR3, respectively, and that RyR3 is much degenerated and almost disappears in adult mammalian skeletal muscles except diaphragm and soleus.2,5,6

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Ogawa, Y. (2007). Dysregulation of the Gain of CICR Through Ryanodine Receptor1 (RyR1): The Putative Mechanism Underlying Malignant Hyperthermia. In: Ebashi, S., Ohtsuki, I. (eds) Regulatory Mechanisms of Striated Muscle Contraction. Advances in Experimental Medicine and Biology, vol 592. Springer, Tokyo. https://doi.org/10.1007/978-4-431-38453-3_24

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