Failure to regulate TNF-induced NF-κB and cell death responses in A20-deficient mice
EG Lee, DL Boone, S Chai, SL Libby, M Chien… - Science, 2000 - science.org
EG Lee, DL Boone, S Chai, SL Libby, M Chien, JP Lodolce, A Ma
Science, 2000•science.orgA20 is a cytoplasmic zinc finger protein that inhibits nuclear factor κB (NF-κB) activity and
tumor necrosis factor (TNF)–mediated programmed cell death (PCD). TNF dramatically
increases A20 messenger RNA expression in all tissues. Mice deficient for A20 develop
severe inflammation and cachexia, are hypersensitive to both lipopolysaccharide and TNF,
and die prematurely. A20-deficient cells fail to terminate TNF-induced NF-κB responses.
These cells are also more susceptible than control cells to undergo TNF-mediated PCD …
tumor necrosis factor (TNF)–mediated programmed cell death (PCD). TNF dramatically
increases A20 messenger RNA expression in all tissues. Mice deficient for A20 develop
severe inflammation and cachexia, are hypersensitive to both lipopolysaccharide and TNF,
and die prematurely. A20-deficient cells fail to terminate TNF-induced NF-κB responses.
These cells are also more susceptible than control cells to undergo TNF-mediated PCD …
A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor κB (NF-κB) activity and tumor necrosis factor (TNF)–mediated programmed cell death (PCD). TNF dramatically increases A20 messenger RNA expression in all tissues. Mice deficient for A20 develop severe inflammation and cachexia, are hypersensitive to both lipopolysaccharide and TNF, and die prematurely. A20-deficient cells fail to terminate TNF-induced NF-κB responses. These cells are also more susceptible than control cells to undergo TNF-mediated PCD. Thus, A20 is critical for limiting inflammation by terminating TNF-induced NF-κB responses in vivo.
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