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Originally published In Press as doi:10.1074/jbc.M212764200 on April 3, 2003

J. Biol. Chem., Vol. 278, Issue 24, 21510-21516, June 13, 2003
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TAF7 (TAFII55) Plays a Role in the Transcription Activation by c-Jun*

Christine Munz a b, Eleni Psichari c d, Dimitris Mandilis c, Anne-Claire Lavigne c e f, Maria Spiliotaki c g, Thomas Oehler a h, Irwin Davidson e, Laszlo Tora e, Peter Angel a i and Alexander Pintzas c j

From the a Division of Signal Transduction and Growth Control, Deutsches Krebforschungszentrum, 69120 Heidelberg, Germany, c Laboratory of Signal Mediated Gene Expression, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, 48 Vassileos Constantinou Avenue, 116 35 Athens, Greece, e Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/ULP, 67404, Illkirch Cedex BP 10142, France

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 for publication, December 16, 2002 , and in revised form, April 2, 2003.

* This work was supported by the European Union through the Training and Mobility of Research network FMRX-CT96-0044 and the Biomed-2 Program, by the Greek Secretariat of Research and Technology, and by grants from the Deutsche Forschungsgemeinschaft and CNRS of France. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

b Present address: Roche Diagnostics, 68305 Mannheim, Germany.

d Present address: Institut Curie, 26, rue d' Ulm, 75248 Paris Cedex 05, France.

f Present address: IPBS 205 route de Narbonne 31077 Toulouse, France.

g Present address: Medical School, University of Athens, Mikras Asias 75, Athens, Greece.

h Present address: Promega GmbH, 68199 Mannheim, Germany.

i To 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.


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