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dc.contributor.authorJones, Edwarden_GB
dc.contributor.authorAdcock, Ian M.en_GB
dc.contributor.authorAhmed, Bushra Y.en_GB
dc.contributor.authorPunchard, Neville A.en_GB
dc.date.accessioned2013-09-23T11:52:08Z
dc.date.available2013-09-23T11:52:08Z
dc.date.issued2007
dc.identifier.citationJones E., Adcock I.M., Ahmed B.Y. and Punchard N. (2007) 'Modulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCε and JAK2 in RAW macrophages', Journal of Inflammation, 4(1), pp.23-42en_GB
dc.identifier.issn1476-9255
dc.identifier.doi10.1186/1476-9255-4-23
dc.identifier.urihttp://hdl.handle.net/10547/302089
dc.description.abstractNuclear factor kappa B (NF-κB) has been shown to play an important role in regulating the expression of many genes involved in cell survival, immunity and in the inflammatory processes. NF-κB activation upregulates inducible nitric oxide synthase leading to enhanced nitric oxide production during an inflammatory response. NF-κB activation is regulated by distinct kinase pathways independent of inhibitor of κB kinase (IKK). Here, we examine the role of protein kinase C isoforms and janus activated kinase 2 (JAK2) activation in NF-κB activation and LPS-stimulated NO production. The results further define the role of NF-κB in LPS stimulated NO production in RAW macrophages. The data support a function for PKCε, JAK2 and p38 MAPK in NF-κB activation following p65 nuclear import.
dc.language.isoenen
dc.publisherBioMed Centralen_GB
dc.relation.urlhttp://www.journal-inflammation.com/content/4/1/23en_GB
dc.rightsArchived with thanks to Journal of Inflammationen_GB
dc.subjectNF-κBen_GB
dc.subjectLPS stimulated NO productionen_GB
dc.subjectp65 nuclear importen_GB
dc.subjectRAW macrophagesen_GB
dc.subjectPKCεen_GB
dc.subjectJAK2en_GB
dc.subjectp38 MAPKen_GB
dc.subjectNF-κB activationen_GB
dc.titleModulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCε and JAK2 in RAW macrophagesen
dc.typeArticleen
dc.contributor.departmentUniversity of East Londonen_GB
dc.contributor.departmentUniversity of Lutonen_GB
dc.identifier.journalJournal of Inflammationen_GB
html.description.abstractNuclear factor kappa B (NF-κB) has been shown to play an important role in regulating the expression of many genes involved in cell survival, immunity and in the inflammatory processes. NF-κB activation upregulates inducible nitric oxide synthase leading to enhanced nitric oxide production during an inflammatory response. NF-κB activation is regulated by distinct kinase pathways independent of inhibitor of κB kinase (IKK). Here, we examine the role of protein kinase C isoforms and janus activated kinase 2 (JAK2) activation in NF-κB activation and LPS-stimulated NO production. The results further define the role of NF-κB in LPS stimulated NO production in RAW macrophages. The data support a function for PKCε, JAK2 and p38 MAPK in NF-κB activation following p65 nuclear import.


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