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Titolo:
Regulation of ryanodine receptors by reactive nitrogen species
Autore:
Eu, JP; Xu, L; Stamler, JS; Meissner, G;
Indirizzi:
DukeNCniv, Med Ctr, Howard Hughes Med Inst, Dept Med,Div Pulm Med, Durham,Duke Univ Durham NC USA 27710 es Med Inst, Dept Med,Div Pulm Med, Durham, Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA Duke Univ DurhamNC USA 27710 d Ctr, Dept Cell Biol, Durham, NC 27710 USA Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 ophys, Chapel Hill, NC 27599 USA Univ N Carolina, Dept Physiol, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 ysiol, Chapel Hill, NC 27599 USA Dukerham,, Med Ctr, Howard Hughes Med Inst, Dept Med,Div Cardiovasc Med, Du Duke Univ Durham NC USA 27710 s Med Inst, Dept Med,Div Cardiovasc Med, Du
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 10, volume: 57, anno: 1999,
pagine: 1079 - 1084
SICI:
0006-2952(19990515)57:10<1079:RORRBR>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; CALCIUM-RELEASE CHANNEL; CYCLIC ADP-RIBOSE; CARDIAC SARCOPLASMIC-RETICULUM; FK506 BINDING-PROTEIN; SKELETAL-MUSCLE; VENTRICULAR MYOCYTES; CA2+ RELEASE; DIFFERENTIAL DISTRIBUTION; ENDOGENOUS EFFECTORS;
Keywords:
Ca2+ release channel; ryanodine receptor; excitation-contraction coupling; cardiac muscle; skeletal muscle; nitric oxide synthase; nitric oxide; reactive nitrogen species;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Meissner, G Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599USA Univ N Carolina Chapel Hill NC USA 27599 l Hill, NC 27599 USA
Citazione:
J.P. Eu et al., "Regulation of ryanodine receptors by reactive nitrogen species", BIOCH PHARM, 57(10), 1999, pp. 1079-1084

Abstract

The ryanodine receptors (RyRs) are large intracellular calcium release channels that play an important role in the control of the calcium levels in excitable and non-excitable cells. Many endogenous modulators such as Mg2+, ATP, or calmodulin can affect the channel activities of the three known mammalian RyR isoforms. RyRs also are known to be redox-responsive. However, the molecular basis and the physiological relevance of redox modulation of RyRs are unclear. Recent evidence suggests that nitric oxide (NO) and related molecules may be endogenous regulators of the: skeletal and cardiac muscle RyRs. The two tissues express nitric oxide syntheses (NOSs), and NO or NO-related species have been shown to affect Ca2+ release channel activities directly via covalent modifications of thiol groups. Both an oxidative and a nitrosative modification of RyRs have been described, leading to either areversible or irreversible alteration of RyR ion channel activity. Additional mechanisms of regulation may include cyclic GMP-dependent signaling pathways and NO modification of RyR regulatory proteins such as the surface membrane L-type Ca2+ channel. Modification of RyRs by NO may influence a variety of physiological functions such as insulin release, vasomotor control, and muscle contraction. (C) 1999 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 08:37:35