Failure to regulate TNF-induced NF-kappa B and cell death responses in A20-deficient mice

Citation
Eg. Lee et al., Failure to regulate TNF-induced NF-kappa B and cell death responses in A20-deficient mice, SCIENCE, 289(5488), 2000, pp. 2350-2354
Citations number
16
Categorie Soggetti
Multidisciplinary,Multidisciplinary,Multidisciplinary
Journal title
SCIENCE
ISSN journal
00368075 → ACNP
Volume
289
Issue
5488
Year of publication
2000
Pages
2350 - 2354
Database
ISI
SICI code
0036-8075(20000929)289:5488<2350:FTRTNB>2.0.ZU;2-H
Abstract
A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor kappa B (NF-kappa B) activity and tumor necrosis factor (TNF)-mediated programme d cell death (PCD). TNF dramatically increases A20 messenger RNA expression in all tissues. Mice deficient far A20 develop severe inflammation and cac hexia, are hypersensitive to both Lipopolysaccharide and TNF, and die prema turely. A20-deficient cells fail to terminate TNF-induced NF-kappa B respon ses. These cells are also more susceptible than control cells to undergo TN F-mediated PCD. Thus, AZO is critical for limiting inflammation by terminat ing TNF-induced NF-kappa B responses in vivo.