![]() |
CiteULike | ![]() |
booker's CiteULike | ![]() |
![]() |
|
![]() |
Register | ![]() |
Log in | ![]() |
A20 and A20-binding proteins as cellular inhibitors of nuclear factor-κB-dependent gene expression and apoptosisby: R. Beyaert
|
Reviews
[Write a review of this article]
Find related articles from these CiteULike users
Find related articles with these CiteULike tags
Posting History
AbstractProper gene expression and cell growth are critical for the survival of all organisms. Nuclear factor-kappaB (NF-κB)-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-κB 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-κB 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.
BibTeX record
RIS record