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

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.

Pubmed ID: 11009421

Authors

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

Journal

Science (New York, N.Y.)

Publication Data

September 29, 2000

Associated Grants

  • Agency: NIGMS NIH HHS, Id: 5T32GM07183
  • Agency: NIDDK NIH HHS, Id: R01 DK052751
  • Agency: NIGMS NIH HHS, Id: T32GM07839

Mesh Terms

  • Animals
  • Apoptosis
  • Cachexia
  • Cells, Cultured
  • Cysteine Endopeptidases
  • DNA
  • DNA-Binding Proteins
  • Fibroblasts
  • Gene Targeting
  • I-kappa B Proteins
  • Inflammation
  • Interleukin-1
  • Intestines
  • Intracellular Signaling Peptides and Proteins
  • Kidney
  • Lipopolysaccharides
  • Liver
  • Mice
  • NF-kappa B
  • Nuclear Proteins
  • Phosphorylation
  • Proteins
  • Skin
  • T-Lymphocytes
  • Tumor Necrosis Factor-alpha
  • Zinc Fingers