TRIM22 inhibits the TRAF6-stimulated NF-κB pathway by targeting TAB2 for degradation

Virol Sin. 2013 Aug;28(4):209-15. doi: 10.1007/s12250-013-3343-4. Epub 2013 Jun 26.

Abstract

Tripartite motif containing 22 (TRIM22), a member of the TRIM/RBCC family, has been reported to activate the nuclear factor-kappa B (NF-κB) pathway in unstimulated macrophage cell lines, but the detailed mechanisms governing this activation remains unclear. We investigated this mechanism in HEK293T cells. We found that overexpression of TRIM22 could activate the NF-κB pathway and conversely, could inhibit the tumor necrosis factor receptor-associated factor 6 (TRAF6)-stimulated NF-κB pathway in HEK293T cells. Further experiments showed that TRIM22 could decrease the self-ubiquitination of TRAF6, and interact with and degrade transforming growth factor-β activated kinase 1 binding protein 2 (TAB2), and that these effects could be partially rescued by a TRIM22 RING domain deletion mutant. Collectively, our data indicate that overexpression of TRIM22 may negatively regulate the TRAF6-stimulated NF-κB pathway by interacting with and degrading TAB2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / antagonists & inhibitors*
  • Cell Line
  • Gene Expression Regulation*
  • Humans
  • Minor Histocompatibility Antigens
  • NF-kappa B / metabolism
  • Repressor Proteins / metabolism*
  • Signal Transduction
  • TNF Receptor-Associated Factor 6 / metabolism*
  • Tripartite Motif Proteins

Substances

  • Adaptor Proteins, Signal Transducing
  • Minor Histocompatibility Antigens
  • NF-kappa B
  • Repressor Proteins
  • TAB2 protein, human
  • TNF Receptor-Associated Factor 6
  • TRIM22 protein, human
  • Tripartite Motif Proteins