Ryanodine receptor acts as a sensor for redox stress.
Ryanoids have not attained importance as insecticides, but the increasing number of xenobiotic effectors known to influence Ca2+ signalling by interaction with ryanodine receptors (RyRs) may serve to identify new targets for insect control. A historical review of redox control of microsomal Ca2+ transport is given here, followed by recent evidence indicating that hyperactive Cys residues are an essential component of a transmembrane redox sensor. Focus is on the role of sulfhydryl chemistry in RyR regulation; metabolic quinonoid intermediates from pesticides and other environmental contaminants are of interest in this context.
Pessah
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Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA 95616, USA. inpessah@ucdavis.edu
D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D002462:Cell Membrane / Q000502:physiology; D008564:Membrane Potentials; D008861:Microsomes / Q000502:physiology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*
D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium