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    Science. 2000 Sep 29;289(5488):2350-4.

    Failure to regulate TNF-induced NF-kappaB and cell death responses in A20-deficient mice.

    Lee EG, Boone DL, Chai S, Libby SL, Chien M, Lodolce JP, Ma A.

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    Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC 6084, Chicago, IL 60637, USA.

    Abstract

    A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor kappaB (NF-kappaB) 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-kappaB 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-kappaB responses in vivo.

    PMID:
    11009421
    [PubMed - indexed for MEDLINE]

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