Review
Cell Death and Differentiation (2006) 13, 759–772. doi:10.1038/sj.cdd.4401838; published online 13 January 2006
Good cop, bad cop: the different faces of NF-
B
Edited by G Kroemer
- 1Division of Gene Regulation and Expression, School of Life Sciences, University of Dundee, MSI/WTB Complex, Dow Street, Dundee, Scotland DD1 5EH, UK
- 2Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA
Correspondence: ND Perkins, Division of Gene Regulation and Expression, School of Life Sciences, University of Dundee, MSI/WTB Complex, Dow Street, Dundee, Scotland DD1 5EH, UK. Tel: +44 1382 385 606; Fax: +44 1382 348 072; E-mail: n.d.perkins@dundee.ac.uk
Received 29 September 2005; Revised 8 November 2005; Accepted 9 November 2005; Published online 13 January 2006.
Abstract
Complexes formed from the nuclear factor
B (NF-
B) family of transcription factors are ubiquitously expressed and are induced by a diverse array of stimuli. This results in their becoming activated in a wide variety of different settings. While the functions of NF-
B in many of these contexts have been the subject of intense research and are now well established, it is also clear that there is great diversity in the effects and consequences of NF-
B activation. NF-
B subunits do not necessarily regulate the same genes, in an identical manner, in all of the different circumstances in which they are induced. This review will discuss the different functions of NF-
B, the pathways that modulate NF-
B subunit activity and, in contrast to its more commonly thought of role as a promoter of cancer cell growth and survival, the ability of NF-
B, under some circumstances, to behave as a tumor suppressor.
Keywords:
NF-
B, cancer, tumor suppressor, signal transduction, phosphorylation, post-translational modification
Abbreviations:
APC, adenomatous polyposis coli; ATM, ataxia telangiectasia mutated; ATR, ATM- and Rad3-related; BAFF, B-cell-activating factor of the TNF family; CDK, cyclin-dependent kinase; CK2, casein kinase II; CYLD, Cylindromatosis; EBV, Epstein–Barr virus; ER, Estrogen Receptor; HDAC, histone deacetylase; HMG, high mobility group; HTLV, human T-lymphotropic virus; I
B, inhibitor of
B; I
B-SR, I
B super-repressor; IAP, inhibitor of apoptosis protein; IKK, I
B kinase; ING4, inhibitor of growth family member 4; IRF, interferon response factor; JNK, Jun N-terminal kinase; LMP-1, latent membrane protein 1; LPS, lipopolysaccharide; MAP, mitogen-activated protein; MnSOD, manganese-superoxide dismutase; IL, interleukin; NEMO, NF-
B essential modifier; NF-
B, nuclear factor
B; NGF, nerve growth factor; NIK, NF-
B-inducing kinase; PI3K, phosphoinositide 3-kinase; PKA, protein kinase A; MSK, mitogen- and stress-activated kinase; PKB, protein kinase B; PP4, protein phosphatase 4; PTEN, phosphatase and tensin homolog deleted on chromosome 10; RHD, Rel homology domain; ROS, reactive oxygen species; RSK1, ribosomal S6 kinase 1; SCC, small cell carcinoma; SCF, Skp1/Cul1/F-box protein; TNF, tumor necrosis factor; UV, ultraviolet; PDGF, platelet-derived growth factor; VEGF, vascular endothelial growth factor
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