REPORT

New targets I—signal transduction

Nuclear factor (NF)-B proteins: therapeutic targets^*

I M Verma

Correspondence to:
Correspondence to:
I M Verma
The Salk Institute, Laboratory of Genetics, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA; verma@salk.edu

Abbreviations: IB, inhibitor of B; IKK, IB kinase; MEF, murine embryonic fibroblast; NF, nuclear factor; NLS, nuclear localisation sequence; NEMO, NF-B essential modulator

Keywords: NF-B proteins; pathways; IKK; NEMO; ubiquitination

The first 150 words of the full text of this article appear below.

Nuclear factor (NF)-B is a key player in the control of both innate and adaptive immunity. NF-B proteins are present in the cytoplasm in association with inhibitory proteins called inhibitors of B (IBs). On activation by a large plethora of inducers, the IB proteins are phosphorylated, ubiquitinated, and subsequently degraded in the proteasomes. Degradation of IBs allows translocation of NF-B into the nucleus and bind to their cognate DNA binding sites to regulate the transcription of large numbers of genes including antimicrobial peptides, cytokines, chemokines, stress response proteins, and antiapoptotic proteins. NF-B activity is essential for lymphocyte survival, activation, and mounting normal immune responses. Constitutive activation of NF-B pathways is often associated with inflammatory diseases like rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and asthma. Better understanding of the regulation of NF-B will provide a platform for . . . [Full text of this article]

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