Cyclic ADP-ribose does not affect cardiac or skeletal muscle ryanodine receptors

Bradley R. Fruen, James R. Mickelson, Nirah H. Shomer, Patricio Velez, Charles F. Louis

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

The cardiac muscle isoform of the ryanodine receptor/Ca2+ release channel (RYR) has been proposed to be an important target of cyclic ADP-ribose (cADPR) action in mammalian cells. However, we now demonstrate that neither cADPR (0.1-5 μM), nor the related metabolites, β-NAD+ (0.1-30 mM) and ADP-ribose (0.1-5 μM), affected cardiac RYR activity as determined by [3H]ryanodine binding to cardiac sarcoplasmic reticulum (SR) vesicles. Similarly, cADPR (1 μM) failed to activate single cardiac RYR channels in planar lipid bilayers. Skeletal muscle SR [3H]ryanodine binding was also unaffected by cADPR (up to 30 μM). These results argue against a direct role for the well-characterized RYRs of cardiac or skeletal muscle in mediating cADPR-activated Ca2+ release.

Original languageEnglish (US)
Pages (from-to)123-126
Number of pages4
JournalFEBS Letters
Volume352
Issue number2
DOIs
StatePublished - Sep 26 1994

Bibliographical note

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

Keywords

  • Ca release channel
  • Cyclic ADP-ribose
  • Ryanodine receptor
  • Sarcoplasmic reticulum

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