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Nuclear factor κB in liver disease
  1. N J GALLAGHER,
  2. L S YOUNG
  1. Institute for Cancer Studies, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TA, UK Email:n.j.gallagher@bham.ac.uk

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The control of gene expression by transcription factors is central to the development and regulated function of multicellular organisms. Perhaps the best understood group of transcription factors is the nuclear factor (NF) κB family, the members of which, in response to activation by a range of extracellular factors, regulate the expression of genes responsible for promoting inflammation and modulating apoptotic responses. Interested readers may wish to refer to a recent review on this topic by Neurath et al.1 NF-κB is composed of homodimers and heterodimers of members of the Rel protein family, the most ubiquitous being p65/RelA which typically heterodimerises with p50 to form active transcription factor complexes. It is not surprising that NF-κB activation is tightly regulated via a cascade of kinase reactions mediated by a multiprotein complex. The key event after stimulation (usually by the binding of cytokines such as tumour necrosis factor (TNF) α and interleukin (IL) 1 to their cell surface receptors) is the phosphorylation and subsequent degradation of inhibitors (I) of κB proteins (IκBα and …

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