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Modulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCε and JAK2 in RAW macrophages

  • Edward Jones
    ,
  • Ian M. Adcock
    ,
  • Bushra Ahmed
    ,
  • Neville A. Punchard
Research Output: Contribution to journal Article Peer-review

Open access

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.

Publication Information

Output type

Research Output: Contribution to journal Article Peer-review

Original language

English

Journal (Volume, Issue Number)

Journal of Inflammation (United States)

Publication milestones

  • Published - 01/01/2007

Publication status

Published - 01/01/2007

ISSN

1078-7852

External Publication IDs

  • handle.net: 10547/302089
  • Scopus: 38349110194