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Constitutive activation of TAK1 by HTLV-1 tax-dependent overexpression of TAB2 induces activation of JNK-ATF2 but not IKK-NF-kappaB.

HTLV-1 Tax oncoprotein induces persistent activation of the transcription factor NF-kappaB and CREB (cAMP-response element-binding protein)/ATF. Transforming growth factor-beta-activated kinase 1 (TAK1) has been shown to play a critical role in these transcription factors. Here, we found that TAK1 was constitutively activated in Tax-positive HTLV-1-transformed T cells. Tax induced persistent overexpression of TAK1-binding protein 2 (TAB2), but not TAB3, which is essential for TAK1 activation. Surprisingly, TAK1 was not involved in the activation of NF-kappaB. On the other hand, JNK and p38 mitogen-activated protein kinases were activated by TAK1. In addition, ATF2, but not CREB, was a target for the TAK1-JNK pathway, and p38 negatively regulated TAK1 activity through TAB1 phosphorylation. These results indicate that Tax-mediated TAK1 activation is important for the activation of ATF2 rather than NF-kappaB.

Pubmed ID: 17626013


  • Suzuki S
  • Singhirunnusorn P
  • Mori A
  • Yamaoka S
  • Kitajima I
  • Saiki I
  • Sakurai H


The Journal of biological chemistry

Publication Data

August 31, 2007

Associated Grants


Mesh Terms

  • Activating Transcription Factor 2
  • Adaptor Proteins, Signal Transducing
  • Cell Line, Transformed
  • Cell Transformation, Viral
  • Cyclic AMP Response Element-Binding Protein
  • Gene Products, tax
  • Humans
  • I-kappa B Kinase
  • MAP Kinase Kinase 4
  • MAP Kinase Kinase Kinases
  • MAP Kinase Signaling System
  • NF-kappa B
  • Phosphorylation
  • Protein Processing, Post-Translational
  • T-Lymphocytes
  • p38 Mitogen-Activated Protein Kinases