TAF7 (TAFII55) Plays a Role in the Transcription Activation by c-Jun*

  1. Alexander Pintzasc,j
  1. aDivision of Signal Transduction and Growth Control, Deutsches Krebforschungszentrum, 69120 Heidelberg, Germany
  2. cLaboratory of Signal Mediated Gene Expression, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, 48 Vassileos Constantinou Avenue, 116 35 Athens, Greece
  3. eInstitut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/ULP, 67404, Illkirch Cedex BP 10142, France
  1. iTo whom correspondence may be addressed: Deutsches Krebforschungszentrum, Division of Signal Transduction and Growth Control (B-0800), Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany. Tel.: 49-6221-42-4570; Fax: 49-6221-42-4554; E-mail: p.angel{at}dkfz.de. j To whom correspondence may be addressed: Laboratory of Signal Mediated Gene Expression, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, 48, Vas. Constantinou Ave., 116 35 Athens, Greece. Tel.: 30210-7273753; Fax: 30210-7273755; E-mail: apint{at}eie.gr.

Abstract

c-Jun is a member of the AP-1 family of transcription factors regulating expression of specific target genes in a variety of cellular processes including proliferation, stress response, and tumorigenicity. In the present study we have analyzed the mechanism of c-Jun function as a transactivator with respect to members of the basal transcription machinery, TATA-binding protein-associated factors (TAFs). We show that one member of the family, human TAF7 (formerly TAFII55), physically interacts with c-Jun through two independent interaction domains, within the N- and C-terminal part of c-Jun. Interaction in vitro correlates with enhanced transactivation function of c-Jun in HEK293 and COS cells in the presence of increasing amounts of TAF7. TAF7 interacts preferentially with DNA-bound phosphorylated c-Jun, suggesting that TAF7 represents a novel c-Jun co-activator mediating activation of AP-1 target genes in response to extracellular signals.

  • Received December 16, 2002.
  • Revision received April 2, 2003.
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This Article

  1. The Journal of Biological Chemistry 278, 21510-21516.
  1. All Versions of this Article:
    1. M212764200v1
    2. 278/24/21510 (most recent)

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