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Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-kappa B activation

  1. Author:
    Iha, H.
    Peloponese, J. M.
    Verstrepen, L.
    Zapart, G.
    Ikeda, F.
    Smith, C. D.
    Starost, M. F.
    Yedavalli, V.
    Heyninck, K.
    Dikic, I.
    Beyaert, R.
    Jeang, K. T.

  2. Author Address

    Iha, Hidekatsu, Peloponese, Jean-Marie, Yedavalli, Venkat, Jeang, Kuan-Teh] NIAID, NIH, Mol Microbiol Lab, Mol Virol Sect, Bethesda, MD 20892 USA. [Verstrepen, Lynn, Heyninck, Karen, Beyaert, Rudi] Univ Ghent VIB, Dept Mol Biomed Res, Unit Mol Signal Transduct Inflammat, B-9052 Ghent, Belgium. [Ikeda, Fumiyo, Dikic, Ivan] Univ Frankfurt, Sch Med, Inst Biochem 2, Frankfurt, Germany. [Smith, C. Dahlem] SAIC Frederick Inc, NCI FCR, Pathol Histotechnol Lab, Frederick, MD USA. [Starost, Matthew F.] NIH, Div Vet Resources, Bethesda, MD 20892 USA. [Iha, Hidekatsu] Oita Univ, Fac Med, Dept Infect Dis, Hasama Yufu, Japan.
    1. Year: 2008
  2. Journal: Embo Journal
    1. 27
    2. 4
    3. Pages: 629-641
  4. Type of Article: Article
  1. Abstract:

    Nuclear factor kappa B (NF-kappa B) is a key mediator of inflammation. Unchecked NF-kappa B 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-1 beta-induced NF-kappa B activation and that binding to mono- and polyubiquitin by a ubiquitin-binding Zn finger domain in TAX1BP1 is needed for TRAF6 association and NF-kappa B 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-1 beta. TAX1BP1(-/-) cells are more highly activated for NF-kappa B than control cells when stimulated with TNF-alpha or IL-1 beta. Mechanistically, TAX1BP1 acts in NF-kappa B signalling as an essential adaptor between A20 and its targets.

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External Sources

  1. PMID: 18239685

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