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Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-kappaB activation.

The EMBO journal | Feb 20, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18239685

Nuclear factor kappa B (NF-kappaB) is a key mediator of inflammation. Unchecked NF-kappaB signalling can engender autoimmune pathologies and cancers. Here, we show that Tax1-binding protein 1 (TAX1BP1) is a negative regulator of TNF-alpha- and IL-1beta-induced NF-kappaB activation and that binding to mono- and polyubiquitin by a ubiquitin-binding Zn finger domain in TAX1BP1 is needed for TRAF6 association and NF-kappaB inhibition. Mice genetically knocked out for TAX1BP1 are born normal, but develop age-dependent inflammatory cardiac valvulitis, die prematurely, and are hypersensitive to low doses of TNF-alpha and IL-1beta. TAX1BP1-/- cells are more highly activated for NF-kappaB than control cells when stimulated with TNF-alpha or IL-1beta. Mechanistically, TAX1BP1 acts in NF-kappaB signalling as an essential adaptor between A20 and its targets.

Pubmed ID: 18239685 RIS Download

Mesh terms: Animals | Cysteine Endopeptidases | Female | GTPase-Activating Proteins | Heart Diseases | Heart Valves | Hypersensitivity | Inflammation | Interleukin-1beta | Intracellular Signaling Peptides and Proteins | Mice | Mice, Inbred C57BL | Mice, Knockout | NF-kappa B | Neoplasm Proteins | TNF Receptor-Associated Factor 6 | Tumor Necrosis Factor-alpha

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Associated grants

  • Agency: NCI NIH HHS, Id: N01-CO-12400
  • Agency: Intramural NIH HHS, Id:

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