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Cyclic ADP-ribose, the ryanodine receptor and Ca2+ release
R Sitsapesan1, S J McGarry, A J Williams
1National Heart and Lung Institute, Imperial College, London, UK.
Trends in Pharmacological Sciences
|November 1, 1995
Summary
Cyclic ADP-ribose (cADPR) triggers calcium release through ryanodine receptors in cells. This review explores cADPR
Area of Science:
- Cellular biology
- Molecular physiology
- Biochemistry
Background:
- Ryanodine-sensitive Ca2+ channels mediate calcium release from intracellular stores in diverse tissues.
- Activation mechanisms of the ryanodine receptor-channel complex are isoform and cell-type specific.
- Channel gating is regulated by a complex interplay of endogenous intracellular compounds.
Purpose of the Study:
- To review the mechanisms of cyclic ADP-ribose (cADPR)-induced Ca2+ release.
- To evaluate the probability that cADPR-activated Ca2+ release involves known ryanodine receptor-Ca2+ channel isoforms.
Main Methods:
- Literature review of studies on ryanodine receptors and Ca2+ signaling.
- Analysis of existing data on cADPR function and ryanodine receptor modulation.
- Comparative discussion of different ryanodine receptor isoforms and their activation pathways.
Main Results:
- cADPR is a potent endogenous modulator of intracellular Ca2+ release.
- Evidence suggests a functional link between cADPR and ryanodine receptor activity.
- The precise isoform of the ryanodine receptor involved in cADPR signaling requires further elucidation.
Conclusions:
- cADPR-mediated Ca2+ release is a significant physiological process.
- Ryanodine receptors are likely mediators of cADPR-induced Ca2+ release.
- Further research is needed to definitively identify the specific ryanodine receptor isoform(s) activated by cADPR.