Please use this identifier to cite or link to this item: https://repositorio.ucb.br:9443/jspui/handle/123456789/7425
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dc.contributor.authorFigueiredo, Florêncio
dc.contributor.authorUhing, Ronald J.
dc.contributor.authorKenji, Okonogi
dc.contributor.authorGettys, Tom W.
dc.contributor.authorJohnson, Stewart P.
dc.contributor.authorAdams, Dolph O
dc.contributor.authorPrpic, Verônica
dc.date.accessioned2016-10-10T03:51:26Z-
dc.date.available2016-10-10T03:51:26Z-
dc.date.issued1990
dc.identifier.citationFIGUEIREDO, Florêncio. et al. Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression. The Journal of Biological Chemistry, v. 165, n. 21, p. 12317-12323, 1990.pt_BR
dc.identifier.issn219258
dc.identifier.urihttp://hdl.handle.net/123456789/202
dc.identifier.urihttps://repositorio.ucb.br:9443/jspui/handle/123456789/7425-
dc.description.abstractThe ability of interferon-gamma (IFN gamma) to increase class II major histocompatibility complex (class II MHC) gene products in murine macrophages involves activation of Na+/H+ exchange (Prpic V., Yu, S. F., Figueiredo, F., Hollenbach, P. W., Gawdi, G., Herman, B., Uhing, R. J., and Adams, D. O. (1989) Science 244, 469-471). The ability of IFN gamma to increase class II MHC gene product expression is inhibited by a variety of agents. In the present studies, the involvement of cAMP-dependent protein kinase in modulating IFN gamma-induced expression of MHC gene products and the mechanism of regulation were assessed in macrophages treated with agents which activated cAMP-dependent protein kinase by different molecular mechanisms. Prostaglandin E2 (PGE2) produced a rapid (within 30 s) dose-dependent elevation of cAMP which was paralleled by the activation of cAMP-dependent protein kinase. The elevation of cAMP by PGE2 was still evident at 1 h and maintained through a 4-h incubation. Concentrations of PGE2 which activated the protein kinase produced a dose-dependent inhibition of surface expression of I-A and transcription of class II MHC genes. Inhibition of IFN gamma-induced class II MHC gene product expression was also observed in macrophages treated with agents which activated cAMP-dependent protein kinase by postreceptor mechanisms. Dibutyryl-cAMP (0.01-1 mM), 25 microM forskolin, 0.1 micrograms/ml cholera toxin, and 3-isobutyl-1-methylxanthine (0.1-1 mM) each suppressed IFN gamma-induced cell surface I-A expression, class II MHC gene transcription, and 22Na+ influx. The results are consistent with the suggestion that activation of cAMP-dependent protein kinase regulates an early transductional event initiated by IFN gamma, perhaps Na+/H+ exchange, which is involved in regulating transcription of class II MHC genes and their subsequent expression.pt_BR
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dc.formatTextopt_BR
dc.language.isoenpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectCiências da saúdept_BR
dc.subjectMedicinapt_BR
dc.subjectPatologia clínicapt_BR
dc.titleActivation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expressionpt_BR
dc.typeArtigopt_BR
dc.description.versionSimpt_BR
dc.description.statusPublicadopt_BR
dc.journalThe Journal of Biological Chemistrypt_BR
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