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Titolo:
CGMP STIMULATION OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR CL- CHANNELS COEXPRESSED WITH CGMP-DEPENDENT PROTEIN-KINASE TYPE-IIBUT NOT TYPE I-BETA
Autore:
VAANDRAGER AB; TILLY BC; SMOLENSKI A; SCHNEIDERRASP S; BOT AGM; EDIXHOVEN M; SCHOLTE BJ; JARCHAU T; WALTER U; LOHMANN SM; POLLER WC; DEJONGE HR;
Indirizzi:
ERASMUS UNIV ROTTERDAM,DEPT BIOCHEM,FAC MED,POB 1738 NL-3000 DR ROTTERDAM NETHERLANDS ERASMUS UNIV ROTTERDAM,FAC MED & HLTH SCI,DEPT CLIN GENET NL-3000 DR ROTTERDAM NETHERLANDS ERASMUS UNIV ROTTERDAM,FAC MED & HLTH SCI,DEPT BIOCHEM,CARDIOVASC RESINST,COEUR NL-3000 DR ROTTERDAM NETHERLANDS MED UNIV CLIN WURZBURG,LAB CLIN BIOCHEM D-97080 WURZBURG GERMANY
Titolo Testata:
The Journal of biological chemistry
fascicolo: 7, volume: 272, anno: 1997,
pagine: 4195 - 4200
SICI:
0021-9258(1997)272:7<4195:CSOCTC>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEAT-STABLE ENTEROTOXIN; INTESTINAL ELECTROLYTE TRANSPORT; CYCLIC-GMP; DIARRHEAL DISEASE; CHLORIDE CHANNELS; GUANYLYL CYCLASE; CELL-LINE; ACTIVATION; RAT; CLONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
A.B. Vaandrager et al., "CGMP STIMULATION OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR CL- CHANNELS COEXPRESSED WITH CGMP-DEPENDENT PROTEIN-KINASE TYPE-IIBUT NOT TYPE I-BETA", The Journal of biological chemistry, 272(7), 1997, pp. 4195-4200

Abstract

In order to investigate the involvement of cGMP-dependent protein kinase (cGK) type II in cGMP-provoked intestinal Cl- secretion, cGMP-dependent activation and phosphorylation of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels was analyzed after expression of cGK II or cGK I beta in intact cells. An intestinal cell line which stably expresses CFTR (IEC-CF7) but contains no detectable endogenous cGK II was infected with a recombinant adenoviral vector containingthe cGK II coding region (Ad-cGK II) resulting in co-expression of active cGK II. In these cells, CFTR was activated by membrane-permeant analogs of cGMP or by the cGMP-elevating hormone atrial natriuretic peptide as measured by I-125(-) efflux assays and whole-cell patch clamp analysis. In contrast, infection with recombinant adenoviruses expressing cGK I beta or luciferase did not convey cGMP sensitivity to CFTR in IEC-CF7 cells. Concordant with the activation of CFTR by only cGK II, infection with Ad-cGK II but not Ad-cGK I beta enabled cGMP analogs to increase CFTR phosphorylation in intact cells. These and other dataprovide evidence that endogenous cGK II is a key mediator of cGMP-provoked activation of CFTR in cells where both proteins are co-localized, e.g. intestinal epithelial cells. Furthermore, they demonstrate thatneither the soluble cGK I beta nor cAMP-dependent protein kinase are able to substitute for cGK II in this cGMP-regulated function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 15:33:51