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Titolo:
The third intracellular loop of the rat and mouse cholecystokinin-A receptors is responsible for different patterns of gene activation
Autore:
Poosti, R; Di Malta, L; Gagne, D; Bernad, N; Galleyrand, JC; Escrieut, C; Silvente-Poirot, S; Fourmy, D; Martinez, J;
Indirizzi:
Fac Pharm Montpellier, Lab Acides Amines Peptides & Prot, CNRS, UMR 5810, F-34060 Montpellier 2, France Fac Pharm Montpellier Montpellier France 2 F-34060 Montpellier 2, France CHU Rangueil, Inst Louis Bugnard, INSERM, U151, Toulouse, France CHU Rangueil Toulouse France is Bugnard, INSERM, U151, Toulouse, France
Titolo Testata:
MOLECULAR PHARMACOLOGY
fascicolo: 6, volume: 58, anno: 2000,
pagine: 1381 - 1388
SICI:
0026-895X(200012)58:6<1381:TTILOT>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
C-FOS GENE; PANCREATIC ACINI; AMYLASE RELEASE; PHOSPHOINOSITIDE BREAKDOWN; INOSITOL PHOSPHATES; MOLECULAR-CLONING; EXPRESSION; CCK; AFFINITY; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Martinez, J Fac Pharm Montpellier, Lab Acides Amines Peptides & Prot, CNRS, UMR 5810, 15 Ave Ch Flahault, F-34060 Montpellier 2, France Fac Pharm Montpellier 15 Ave Ch Flahault Montpellier France 2
Citazione:
R. Poosti et al., "The third intracellular loop of the rat and mouse cholecystokinin-A receptors is responsible for different patterns of gene activation", MOLEC PHARM, 58(6), 2000, pp. 1381-1388

Abstract

It has previously been reported that the cholecystokinin analog JMV-180 behaves differently on the rat and the mouse cholecystokinin-A receptor (CCK-AR). In mice this analog acts as an agonist on low- and high-affinity sitesof the CCK-AR, whereas in rats this compound acts as an agonist on high-affinity sites and as an antagonist on low- affinity sites. In an attempt to understand why the same compound behaves differently on these two CCK-A receptors, we cloned the cDNA encoding the mouse CCK-AR. We then investigated a cellular model able to mimic the effect that was observed in rats and mice. HeLa cells were transiently cotransfected with plasmids leading to expression of the rat or mouse CCK-AR in the presence of pFos-Luc as reporter plasmid; such a plasmid placed the regulatory part of the human c-Fos gene upstream from the firefly luciferase structural gene (Luc). We then observed that the two CCK-A receptors behaved differently, not only in the presence of compound JMV-180 but also in the presence of cholecystokinin or even in absence of ligand; the rat CCK-AR was 2 to 3 times more potent than the mouse CCK-AR in inducing the reporter protein, whatever the ligand studied. This result was confirmed using the same kind of experiment with the reporterplasmid p(TRE)(3)-tk-Luc. Using various mutated receptors, we investigatedthe role of the putative third intracellular loop. We concluded that both the primary structure of the receptor and the cellular context are in part responsible for the differential behavior of these CCK-A receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 13:44:58