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Titolo:
AGONIST-STIMULATED CYCLIC ADP RIBOSE - ENDOGENOUS MODULATOR OF CA2-INDUCED CA2+ RELEASE IN INTESTINAL LONGITUDINAL MUSCLE()
Autore:
KUEMMERLE JF; MAKHLOUF GM;
Indirizzi:
VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,POB 980711 RICHMOND VA 23298
Titolo Testata:
The Journal of biological chemistry
fascicolo: 43, volume: 270, anno: 1995,
pagine: 25488 - 25494
SICI:
0021-9258(1995)270:43<25488:ACAR-E>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
LYMPHOCYTE ANTIGEN CD38; INDUCED CALCIUM-RELEASE; SEA-URCHIN EGGS; INOSITOL TRISPHOSPHATE; BETA-CELLS; RYANODINE; ENZYME; METABOLITE; RECEPTORS; NAD+;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
J.F. Kuemmerle e G.M. Makhlouf, "AGONIST-STIMULATED CYCLIC ADP RIBOSE - ENDOGENOUS MODULATOR OF CA2-INDUCED CA2+ RELEASE IN INTESTINAL LONGITUDINAL MUSCLE()", The Journal of biological chemistry, 270(43), 1995, pp. 25488-25494

Abstract

We have previously shown that agonist-induced Ca2+ mobilization in intestinal longitudinal muscle is mediated by ryanodine-sensitive, inositol 1,4,5-trisphosphate-insensitive sarcoplasmic Ca2+ channels. Ca2+ release via these channels is triggered by agonist-stimulated Ca2+ influx and results in Ca2+-induced Ca2+ release. The present study examined whether cyclic ADP-ribose (cADPR) is synthesized in response to stimulation of longitudinal muscle by agonists and modulates the activity of Ca2+ release channels. Cyclic ADPR bound with high affinity to dispersed longitudinal muscle cells (IC50 1.9 nM) and induced Ca2+ release(EC(50) 3.8 nM), increase in lCa(2+)](i) (EC(50) 2.0 nM), and contraction (EC(50) 1.1 nM); cADPR had no effect on circular muscle cells. The effects of cADPR were blocked by ruthenium red, dantrolene, and the specific antagonist, 8-amino-cADPR, and were augmented by caffeine butnot affected by heparin. The binding of cADPR and its ability to stimulate Ca2+ release were dependent on the concentration of Ca2+. CyclicADPR was capable of stimulating Ca2+ release at subthreshold Ca2+ concentrations (25-100 nM) and of enhancing Ca2+-induced Ca2+ release. Longitudinal muscle extracts incubated with beta-NAD(+) produced a time-dependent increase in Ca2+-mobilizing activity identified as authenticcADPR by blockade of Ca2+ release with 8-amino-cADPR and ruthenium red. Ca2+ mobilizing activity was increased by cholecystokinin octapeptide (CCK-8) in a concentration-dependent fashion. The increase induced by CCK-8 was suppressed by the CCK-A antagonist, L364,718, nifedipine,and guanyl-5'-yl thiophosphate. The study shows that ADP-ribosyl cyclase can be stimulated by agonists and that cADPR can act as an endogenous modulator of Ca2+-induced Ca2+ release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:36:03