title: [Modulation of the action of interferon-gamma by protein G].
abstract: These studies were designed to investigate the characteristics of the intracellular second messengers induced by interferons (IFN-alpha/beta and IFN-gamma) after receptor binding. Pretreatment of target cells with V. cholerae toxin, which is Known to activate the GTP-binding stimulatory protein (Gs), potentiated the action of IFN-gamma, but not of IFN-alpha/beta. By contrast, B. pertussis toxin, which is known to act on the GTP-binding inhibitory protein (Gi doesn't affect the action of both IFN) (Gi). Besides this forskolin and PGE1, known to increase intracellular cAMP levels, completely prevented antiviral state induction by IFN-gamma, but had no effects on IFN-alpha/beta. Altogether these results demonstrate that IFN-gamma transduction signal is mediated by a G protein with functional characteristics similar to those of the known Gs protein.
authors.affiliation: Istituto di Microbiologia, Università di Torino, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Gariglio
authors.forename: G
authors.initials: G
authors.lastname: Cavallo
authors.forename: S
authors.initials: S
authors.lastname: Landolfo
mesh_terms: D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D002772:Cholera Toxin / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D004347:Drug Interactions; D019204:GTP-Binding Proteins / Q000494:pharmacology*; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism*; D051379:Mice; D037342:Pertussis Toxin; D011971:Receptors, Immunologic / Q000187:drug effects; D017471:Receptors, Interferon; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
chemical_list: D011971:Receptors, Immunologic; D017471:Receptors, Interferon; D010566:Virulence Factors, Bordetella; D005576:Colforsin; D007371:Interferon-gamma; D002772:Cholera Toxin; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins; D000527:Alprostadil
vernacular_title: Modulazione della risposta all'IFN-gamma da parte delle proteine G.