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dc.contributor.authorKravchenko, V. V.zh_CN
dc.contributor.authorPan, Z. X.zh_CN
dc.contributor.authorHan, J. H.zh_CN
dc.contributor.authorHerbert, J. M.zh_CN
dc.contributor.authorUlevitch, R. J.zh_CN
dc.contributor.authorYe, R. D.zh_CN
dc.contributor.author韩家淮zh_CN
dc.date.accessioned2013-12-12T02:24:44Z
dc.date.available2013-12-12T02:24:44Z
dc.date.issued1995zh_CN
dc.identifier.citationJournal of Biological Chemistry,270(25):14928-14934zh_CN
dc.identifier.issn0021-9258zh_CN
dc.identifier.otherISI:A1995RE66600016zh_CN
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/65839
dc.description.abstractThe capability of platelet activating factor (PAF) to induce transcription factor activation was examined. In stably transfected Chinese hamster ovary cells expressing the PAF receptor (CHO PAFR), PAF stimulation resulted in the nuclear expression of a DNA binding activity with specificity to the kappa B sequence. The p50 and p65 proteins, constituents of the prototypic nuclear factor kappa B (NF-kappa B), were identified as components of the DNA . protein complexes by antipeptide antibodies in gel supershift as well as UV cross-linking experiments. PAF induced an initial decrease and subsequent increase of cytoplasmic I kappa B alpha levels, accompanied by up-regulation of the I kappa B alpha messenger RNA, a feature of NF-kappa B activation. PAF-induced kappa B binding activity was detected within 15 min after agonist stimulation, peaked at 30-40 min, and remained detectable by 2.5 h. SR 27417, a PAF receptor antagonist, blocked PAF-induced kappa B binding activity but not that induced by tumor necrosis factor-alpha (TNF alpha). Cholera toxin treatment markedly reduced PAF-induced kappa B binding activity, whereas pertussis toxin had no significant inhibitory effect. Neither of the two toxins affected the kappa B binding activity induced by TNF alpha in the same cells. In addition to the CHO-PAFR cells, PAF stimulated kappa B binding activity in the murine P388D(1) macrophage and the human ASK.0 B cell lines that express endogenous PAF receptors. These results imply a potential role of PAF in the regulation of gene expression through a G protein-coupled transcription factor activation pathway.zh_CN
dc.language.isoen_USzh_CN
dc.subjectSIGNAL TRANSDUCTION MECHANISMSzh_CN
dc.subjectHUMAN-IMMUNODEFICIENCY-VIRUSzh_CN
dc.subjectFACTOR RECEPTORzh_CN
dc.subjectTRANSCRIPTION FACTORzh_CN
dc.subjectSURFACE EXPRESSIONzh_CN
dc.subjectEPITHELIAL-CELLSzh_CN
dc.subjectBINDING PROTEINSzh_CN
dc.subjectLIGAND-BINDINGzh_CN
dc.subjectT-CELLSzh_CN
dc.subjectLIPOPOLYSACCHARIDEzh_CN
dc.titlePLATELET-ACTIVATING-FACTOR INDUCES NF-KAPPA-B ACTIVATION THROUGH A G-PROTEIN-COUPLED PATHWAYzh_CN
dc.typeArticlezh_CN


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