Please use this identifier to cite or link to this item: https://dspace.iiti.ac.in/handle/123456789/4018
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dc.contributor.authorSrivastava, Mansien_US
dc.contributor.authorBaig, Mirza Saqiben_US
dc.date.accessioned2022-03-17T01:00:00Z-
dc.date.accessioned2022-03-17T15:31:22Z-
dc.date.available2022-03-17T01:00:00Z-
dc.date.available2022-03-17T15:31:22Z-
dc.date.issued2018-
dc.identifier.citationSrivastava, M., & Baig, M. S. (2018). NOS1 mediates AP1 nuclear translocation and inflammatory response. Biomedicine and Pharmacotherapy, 102, 839-847. doi:10.1016/j.biopha.2018.03.069en_US
dc.identifier.issn0753-3322-
dc.identifier.otherEID(2-s2.0-85054421405)-
dc.identifier.urihttps://doi.org/10.1016/j.biopha.2018.03.069-
dc.identifier.urihttps://dspace.iiti.ac.in/handle/123456789/4018-
dc.description.abstractA hallmark of the AP1 functioning is its nuclear translocation, which induces proinflammatory cytokine expression and hence the inflammatory response. After endotoxin shock AP1 transcription factor, which comprises Jun, ATF2, and Fos family of proteins, translocates into the nucleus and induces proinflammatory cytokine expression. In the current study, we found, NOS1 inhibition prevents nuclear translocation of the AP1 transcription factor subunits. Pharmacological inhibition of NOS1 impedes translocation of subunits into the nucleus, suppressing the transcription of inflammatory genes causing a diminished inflammatory response. In conclusion, the study shows the novel mechanism of NOS1- mediated AP1 nuclear translocation, which needs to be further explored. © 2018 Elsevier Masson SASen_US
dc.language.isoenen_US
dc.publisherElsevier Masson SASen_US
dc.sourceBiomedicine and Pharmacotherapyen_US
dc.subjectactivating transcription factor 2en_US
dc.subjectimmunoglobulin enhancer binding proteinen_US
dc.subjectinterleukin 8en_US
dc.subjectneuronal nitric oxide synthaseen_US
dc.subjectnitric oxideen_US
dc.subjectnitric oxide synthaseen_US
dc.subjectnitriteen_US
dc.subjectprotein c junen_US
dc.subjectprotein fosen_US
dc.subjectsynaptotagmin Ien_US
dc.subjecttoll like receptor 4en_US
dc.subjecttranscription factor AP 1en_US
dc.subjectautacoiden_US
dc.subjectcytokineen_US
dc.subjectinducible nitric oxide synthaseen_US
dc.subjectinterleukin 1 receptoren_US
dc.subjectlipopolysaccharideen_US
dc.subjectmembrane proteinen_US
dc.subjectneuronal nitric oxide synthaseen_US
dc.subjectnitric oxideen_US
dc.subjectprotein c junen_US
dc.subjectTIRAP protein, mouseen_US
dc.subjecttranscription factor AP 1en_US
dc.subjectanimal cellen_US
dc.subjectanimal experimenten_US
dc.subjectanimal modelen_US
dc.subjectArticleen_US
dc.subjectbone marrow derived macrophageen_US
dc.subjectcontrolled studyen_US
dc.subjectcytokine responseen_US
dc.subjectenzyme inhibitionen_US
dc.subjectgene controlen_US
dc.subjectimmune responseen_US
dc.subjectinflammationen_US
dc.subjectmacrophageen_US
dc.subjectmouseen_US
dc.subjectnonhumanen_US
dc.subjectpriority journalen_US
dc.subjectprotein expressionen_US
dc.subjectprotein protein interactionen_US
dc.subjectprotein transporten_US
dc.subjectquantitative analysisen_US
dc.subjectanimalen_US
dc.subjectcell nucleusen_US
dc.subjectdrug effecten_US
dc.subjectgene expression regulationen_US
dc.subjectinflammationen_US
dc.subjectmetabolismen_US
dc.subjectpathologyen_US
dc.subjectprotein subuniten_US
dc.subjectprotein transporten_US
dc.subjectAnimalsen_US
dc.subjectCell Nucleusen_US
dc.subjectCytokinesen_US
dc.subjectGene Expression Regulationen_US
dc.subjectInflammationen_US
dc.subjectInflammation Mediatorsen_US
dc.subjectLipopolysaccharidesen_US
dc.subjectMacrophagesen_US
dc.subjectMembrane Glycoproteinsen_US
dc.subjectMiceen_US
dc.subjectNitric Oxideen_US
dc.subjectNitric Oxide Synthase Type Ien_US
dc.subjectNitric Oxide Synthase Type IIen_US
dc.subjectProtein Subunitsen_US
dc.subjectProtein Transporten_US
dc.subjectProto-Oncogene Proteins c-junen_US
dc.subjectReceptors, Interleukin-1en_US
dc.subjectTranscription Factor AP-1en_US
dc.titleNOS1 mediates AP1 nuclear translocation and inflammatory responseen_US
dc.typeJournal Articleen_US
Appears in Collections:Department of Biosciences and Biomedical Engineering

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