Apr 1, 2013

Role of nuclear IκBs in inflammation regulation

Biomolecular Concepts
Tomoki ChibaTakehito Sato

Abstract

A wide variety of environmental cues, including inflammatory cytokines, ligands for pattern recognition receptors and endogenous danger signals, activate the inducible transcription factor nuclear factor-κB (NF-κB), which is a central regulator of inflammatory and immune responses. Excessive activation of NF-κB results in the development of severe diseases, such as chronic inflammatory disorders, autoimmune diseases and cancer. Therefore, the transcriptional activity of NF-κB is tightly regulated at multiple steps. One mechanism is mediated by the inhibitor of κB (IκB), a well-defined regulator of NF-κB that resides in the cytoplasm and prevents NF-κB from nuclear entry by sequestration. Recently, several atypical IκBs that reside in the nucleus were identified: Bcl-3, IκBζ, IκBNS and IκBη. In contrast to conventional IκBs, these atypical IκBs positively and negatively modulate NF-κB-mediated transcription. The function of atypical IκBs is independent of the prevention of NF-κB nuclear entry. Therefore, atypical IκBs are considered distinct from conventional IκBs and have been termed 'nuclear IκBs.' In addition to these members, our recent study indicated that IκBL, originally reported as a susceptibility gene for rheumatoid ar...Continue Reading

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Mentioned in this Paper

Immune Response
Pathogenic Aspects
Transcriptional Regulation
Pathogenesis
Systemic Inflammatory Response Syndrome
Cancer-Predisposing Gene
Transcription, Genetic
I-kappa B Proteins
Cell Nucleus
Rheumatoid Arthritis

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