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Biochem Pharmacol. 2000 Oct 15;60(8):1143-51.

A20 and A20-binding proteins as cellular inhibitors of nuclear factor-kappa B-dependent gene expression and apoptosis.

Author information

1
Unit of Molecular Signal Transduction in Inflammation, Department of Molecular Biology, Ghent University, Ghent, Belgium. rudi@dmb.rug.ac.be

Abstract

Proper gene expression and cell growth are critical for the survival of all organisms. Nuclear factor-kappa B (NF-kappa B)-dependent gene expression and apoptosis play crucial roles in numerous cellular processes, and defects in their regulation may contribute to a variety of diseases including inflammation and cancer. Although there has recently been tremendous progress in our understanding of the signaling pathways that lead to NF-kappa B activation and apoptosis, signaling mechanisms that negatively regulate these processes are only partially understood. This review deals with the zinc finger protein A20, which has been characterized as a dual inhibitor of NF-kappa B activation and apoptosis. Its inducible expression by a wide variety of stimuli, including cytokines such as tumor necrosis factor, interleukin-1, and CD40, as well as bacterial and viral products such as lipopolysaccharide, Epstein-Barr virus latent membrane protein 1, and human T-cell leukemia virus type I Tax, suggests that it is involved in the negative feedback regulation of signaling. We will discuss the possible underlying mechanisms, placing emphasis on the role of several A20-binding proteins that have recently been described. Moreover, evidence is presented that A20 and A20-binding proteins are potential novel therapeutic tools in the treatment of a variety of diseases.

PMID:
11007952
DOI:
10.1016/s0006-2952(00)00404-4
[Indexed for MEDLINE]

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