HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein

Qingsheng Yu, Yasumasa Minoda, Ryoko Yoshida, Hideyuki Yoshida, Hidekatsu Iha, Takashi Kobayashi, Akihiko Yoshimura, Giichi Takaesu

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)


Human T cell leukemia virus type 1 (HTLV-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of HTLV-1-infected T lymphocytes. It has recently been reported that Tax activates a MAPKKK family, TAK1. However, the molecular mechanism of Tax-mediated TAK1 activation is not well understood. In this report, we investigated the role of TAK1-binding protein 2 (TAB2) in Tax-mediated TAK1 activation. We found that TAB2 physically interacts with Tax and augments Tax-induced NF-κB activity. Tax and TAB2 cooperatively activate TAK1 when they are coexpressed. Furthermore, TAK1 activation by Tax requires TAB2 binding as well as ubiquitination of Tax. We also found that the overexpression of TRAF2, 5, or 6 strongly induces Tax ubiquitination. These results suggest that TAB2 may be critically involved in Tax-mediated activation of TAK1 and that NF-κB-activating TRAF family proteins are potential cellular E3 ubiquitin ligases toward Tax.

Original languageEnglish
Pages (from-to)189-194
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - 2008 Jan 4
Externally publishedYes


  • Adapter protein
  • HTLV-1
  • MAP3K
  • NF-κB
  • TAK1
  • TRAF
  • Tax
  • Ubiquitination

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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