TRAF6 regulates proliferation and differentiation of skeletal myoblasts

Tobias Mueck, Felicitas Berger, Ingrid Buechsler, Ralitsa S. Valchanova, Lorena Landuzzi, Pier Luigi Lollini, Karin Klingel, Barbara Munz

Research output: Contribution to journalArticlepeer-review


We could recently demonstrate an important role of receptor interacting protein-2 (RIP2), an activator of nuclear factor kappa B (NF-κB) and a target of activated receptors of the tumor necrosis factor receptor (TNFR) type, in myogenic differentiation and regeneration. Here, we analyze a potential role of TNFR associated factor 6 (TRAF6), which also associates with the cytoplasmic domain of TNFR type, but also IL-1-R and TLR type receptors, and activates NF-κB, in these processes. Specifically, we show that during myogenic differentiation in vitro, traf6 gene expression is downregulated in normal myoblasts, but not in rhabdomyosarcoma cells, suggesting a role of the TRAF6 protein in this process. Inhibition of traf6 expression using specific siRNAs led to an inhibition of both myoblast proliferation and differentiation, whereas inhibition of the TRAF6 effector NF-κB alone in our system only blocked proliferation. Finally, we demonstrate that the traf6 gene is downregulated in skeletal muscle tissue of the dystrophic mdx mouse. Taken together, these data argue for a role of TRAF6 in the regulation of skeletal muscle differentiation and regeneration.

Original languageEnglish
Pages (from-to)99-106
Number of pages8
Issue number2
Publication statusPublished - Feb 2011


  • Myogenic differentiation
  • Rhabdomyosarcoma
  • TRAF6

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology
  • Molecular Biology
  • Cancer Research


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