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Science 9 January 1998:
Vol. 279. no. 5348, pp. 234 - 237
DOI: 10.1126/science.279.5348.234
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Reports

Activation of the Cardiac Calcium Release Channel (Ryanodine Receptor) by Poly-S-Nitrosylation

Le Xu, * Jerry P. Eu, * Gerhard Meissner, dagger Jonathan S. Stamler dagger

Several ion channels are reportedly redox responsive, but the molecular basis for the changes in activity is not known. The mechanism of nitric oxide action on the cardiac calcium release channel (ryanodine receptor) (CRC) in canines was explored. This tetrameric channel contains ~84 free thiols and is S-nitrosylated in vivo. S-Nitrosylation of up to 12 sites (3 per CRC subunit) led to progressive channel activation that was reversed by denitrosylation. In contrast, oxidation of 20 to 24 thiols per CRC (5 or 6 per subunit) had no effect on channel function. Oxidation of additional thiols (or of another class of thiols) produced irreversible activation. The CRC thus appears to be regulated by poly-S-nitrosylation (multiple covalent attachments), whereas oxidation can lead to loss of control. These results reveal that ion channels can differentiate nitrosative from oxidative signals and indicate that the CRC is regulated by posttranslational chemical modification(s) of sulfurs.

L. Xu and G. Meissner, Departments of Biochemistry and Biophysics, and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA.
J. P. Eu and J. S. Stamler, Howard Hughes Medical Institute, Department of Medicine, Divisions of Pulmonary and Cardiovascular Medicine and Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
*   These authors contributed equally to this work.

dagger    To whom correspondence should be addressed.

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   Abstract »    Full Text »    PDF »
Modulation of cardiac contraction, relaxation and rate by the endothelial nitric oxide synthase (eNOS): lessons from genetically modified mice.
P B Massion and J-L Balligand (2003)
J. Physiol. 546, 63-75
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Nitric oxide and myocardial function in heart failure: friend or foe?.
J M Cotton, M T Kearney, and A M Shah (2002)
Heart 88, 564-566
   Abstract »    Full Text »    PDF »
Nitric oxide inhibits ADP-ribosyl cyclase through a cGMP-independent pathway in airway smooth muscle.
T. A. White, T. F. Walseth, and M. S. Kannan (2002)
Am J Physiol Lung Cell Mol Physiol 283, L1065-L1071
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Regulation of Mammalian Liver Methionine Adenosyltransferase.
F. J. Corrales, I. Perez-Mato, M. M. Sanchez del Pino, F. Ruiz, C. Castro, E. R. Garcia-Trevijano, U. Latasa, M. L. Martinez-Chantar, A. Martinez-Cruz, M. A. Avila, et al. (2002)
J. Nutr. 132, 2377S-2381
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Isoforms of Mammalian Adenylyl Cyclase: Multiplicities of Signaling.
R. K. Sunahara and R. Taussig (2002)
Mol. Interv. 2, 168-184
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The Ryanodine Receptor Calcium Channel of {beta}-Cells: Molecular Regulation and Physiological Significance.
M. S. Islam (2002)
Diabetes 51, 1299-1309
   Abstract »    Full Text »    PDF »
Role of cyclic GMP-dependent protein kinase in the contractile response to exogenous nitric oxide in rat cardiac myocytes.
J. Layland, J.-M. Li, and A. M Shah (2002)
J. Physiol. 540, 457-467
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NO donors potentiate the {beta}-adrenergic stimulation of ICa,L and the muscarinic activation of IK,ACh in rat cardiac myocytes.
N. Abi-Gerges, G. Szabo, A. S Otero, R. Fischmeister, and P.-F. Mery (2002)
J. Physiol. 540, 411-424
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Imbalance Between Xanthine Oxidase and Nitric Oxide Synthase Signaling Pathways Underlies Mechanoenergetic Uncoupling in the Failing Heart.
W. F. Saavedra, N. Paolocci, M. E. St. John, M. W. Skaf, G. C. Stewart, J.-S. Xie, R. W. Harrison, J. Zeichner, D. Mudrick, E. Marban, et al. (2002)
Circ. Res. 90, 297-304
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