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  • Original Paper
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Functional cooperation between JunD and NF-κB in rat hepatocytes

Oncogene volume 20, pages 5132–5142 (2001)Cite this article

Abstract

AP-1 and NF-κB are rapidly activated during liver regeneration. Whether these parallel inductions have potential functional implications is not known. Isolated rat hepatocytes were stimulated with two mitogens, epidermal growth factor or hepatocyte growth factor and with tumor necrosis factor α, a cytokine involved in the liver regenerative response in vivo and a strong inducer of NF-κB. All three cytokines increased AP-1 and NF-κB binding to their cognate cis-element and induced a 2.5-fold activation of NF-κB-dependent transcription. Inactivation of AP-1 by TAM67, a dominant negative mutant of AP-1 drastically inhibited basal and cytokine-induced NF-κB transactivation. Overexpression of Jun D, but not of the other Jun or Fos proteins increased by threefold NF-κB transactivation. Functional cooperation between JunD and p65 was demonstrated in a simple Gal-hybrid system. Finally, a twofold decrease in NF-κB transactivation was found in hepatocytes isolated from JunD−/− mice compared with hepatocytes from JunD+/+ mice. Altogether these data demonstrate a functional cooperation of p65 with JunD, a major constituent of AP-1 in normal hepatocytes.

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Acknowledgements

We thank K Blender, B Binetruy, R Weil, J Birrer, JW Lee, XF Wang, A Israël and G Cherqui for providing plasmids and M Yaniv for helpful discussions.

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Authors and Affiliations

  1. Laboratoire de Biologie cellulaire, INSERM U 327, Faculté de Médecine Xavier Bichat et Université Paris 7 Denis Diderot, Paris, France

    Mohamed Rahmani, Philippe Péron, Bernard Lardeux & Dominique Bernuau

  2. Département des Biotechnologies, Unité des Virus Oncogènes, URA 1644 du CNRS, Institut Pasteur, Paris, France

    Jonathan Weitzman & Latifa Bakiri

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  1. Mohamed Rahmani
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Correspondence to Dominique Bernuau.

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Rahmani, M., Péron, P., Weitzman, J. et al. Functional cooperation between JunD and NF-κB in rat hepatocytes. Oncogene 20, 5132–5142 (2001). https://doi.org/10.1038/sj.onc.1204678

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