Modulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCε and JAK2 in RAW macrophages
dc.contributor.author | Jones, Edward | en_GB |
dc.contributor.author | Adcock, Ian M. | en_GB |
dc.contributor.author | Ahmed, Bushra Y. | en_GB |
dc.contributor.author | Punchard, Neville A. | en_GB |
dc.date.accessioned | 2013-09-23T11:52:08Z | |
dc.date.available | 2013-09-23T11:52:08Z | |
dc.date.issued | 2007 | |
dc.identifier.citation | Jones 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.23-42 | en_GB |
dc.identifier.issn | 1476-9255 | |
dc.identifier.doi | 10.1186/1476-9255-4-23 | |
dc.identifier.uri | http://hdl.handle.net/10547/302089 | |
dc.description.abstract | Nuclear 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.iso | en | en |
dc.publisher | BioMed Central | en_GB |
dc.relation.url | http://www.journal-inflammation.com/content/4/1/23 | en_GB |
dc.rights | Archived with thanks to Journal of Inflammation | en_GB |
dc.subject | NF-κB | en_GB |
dc.subject | LPS stimulated NO production | en_GB |
dc.subject | p65 nuclear import | en_GB |
dc.subject | RAW macrophages | en_GB |
dc.subject | PKCε | en_GB |
dc.subject | JAK2 | en_GB |
dc.subject | p38 MAPK | en_GB |
dc.subject | NF-κB activation | en_GB |
dc.title | Modulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCε and JAK2 in RAW macrophages | en |
dc.type | Article | en |
dc.contributor.department | University of East London | en_GB |
dc.contributor.department | University of Luton | en_GB |
dc.identifier.journal | Journal of Inflammation | en_GB |
html.description.abstract | Nuclear 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. |