Roles of c-Rel signalling in inflammation and disease

被引:32
作者
Fullard, Nicola [1 ]
Wilson, Caroline L. [1 ]
Oakley, Fiona [1 ]
机构
[1] Newcastle Univ, Inst Cellular Med, Fibrosis Lab, Liver Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
c-Rel; Inflammation; Immunity; Disease; Pathology; NF-KAPPA-B; GENOME-WIDE ASSOCIATION; TRANSCRIPTION FACTOR REL; TATA-BINDING PROTEIN; T-CELLS; SUSCEPTIBILITY LOCI; GENE-EXPRESSION; LYMPHOCYTE-PROLIFERATION; TRANSACTIVATION DOMAIN; DISTINCT ROLES;
D O I
10.1016/j.biocel.2012.02.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nuclear factor kappa B (NF kappa B) is a dimeric transcription factor comprised of five family members RelA (p65), RelB, c-Rel, p50 and p52. NF kappa B signalling is complex and controls a myriad of normal cellular functions. However, constitutive or aberrant activation of this pathway is associated with disease progression and cancer in multiple organs. The diverse array of biological responses is modulated by many factors, including the activating stimulus, recruitment of co-regulatory molecules, consensus DNA binding sequence, dimer composition and post-translational modifications. Each subunit has very different biological functions and in the context of disease the individual subunits forming the NF kappa B dimer can have a profound effect, causing a shift in the balance from normal to pathogenic signalling. Here we discuss the role of c-Rel dependant signalling in normal physiology and its contribution to disease both inside and outside of the immune system. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:851 / 860
页数:10
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