Potentiation of Smad transactivation by Jun proteins during a combined treatment with epidermal growth factor and transforming growth factor-beta in rat hepatocytes. role of phosphatidylinositol 3-kinase-induced AP-1 activation.

@article{Pron2001PotentiationOS,
  title={Potentiation of Smad transactivation by Jun proteins during a combined treatment with epidermal growth factor and transforming growth factor-beta in rat hepatocytes. role of phosphatidylinositol 3-kinase-induced AP-1 activation.},
  author={Philippe P{\'e}ron and Mohamed Rahmani and Yvrick Zagar and Anne-Marie Durand-Schneider and Bernard Lardeux and Dominique Bernuau},
  journal={The Journal of biological chemistry},
  year={2001},
  volume={276 13},
  pages={10524-31}
}
Cross-talk between Smad and mitogen-activated protein kinase pathways has been described recently, and evidence for Smad cooperation with AP-1 is emerging. Here we report that epidermal growth factor (EGF) potentializes transforming growth factor beta (TGF-beta)-induced Smad3 transactivation in rat hepatocytes, an effect abrogated by TAM-67, a dominant negative mutant of AP-1. Antisense transfection experiments indicated that c-Jun and JunB were involved in the synergistic effect, and… CONTINUE READING
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