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Blood, 1 July 2004, Vol. 104, No. 1, pp. 256-262. Prepublished online as a Blood First Edition Paper on March 18, 2004; DOI 10.1182/blood-2003-08-2661. This Article Full Text (PDF) All Versions of this Article: 2003-08-2661v1 104/1/256    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Benasciutti, E. Articles by Crippa, M. P Search for Related Content PubMed PubMed Citation Articles by Benasciutti, E. Articles by Crippa, M. P Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 5, 2003 Accepted March 4, 2004 MAPK and JNK transduction pathways can phosphorylate Sp1 to activate the uPA minimal promoter elements and endogenous gene transcription Elisa Benasciutti, Gilles Pages, Olga Kenzior, William Folk, Francesco Blasi, and Massimo P Crippa* Centre Antoine Lacassagne, Institute of Signaling, Developmental Biology and Cancer Research, Nice, France Biochemistry Department, University of Missouri-Columbia, Columbia, Missouri, USA Laboratory of Molecular Genetics, S. Raffaele Scientific Institute and Universita Vita-Salute S. Raffaele, Milano, Italy * Corresponding author; email: crippa.massimo{at}hsr.it. Two upstream regions of the human urokinase (uPA) gene regulate its transcription: the minimal promoter (MP) and the enhancer element. The activity of the minimal promoter is essential for basal uPA transcription in prostate adenocarcinoma PC3 cells. Binding of a phosphorylated Sp1 transcription factor is, in turn, essential for the activity of the MP. Here we report that the JNK pathway is required for the basal activity of the MP and for the expression of the endogenous uPA gene in PC3 cells and for activated transcription in LNCaP cells. On the other hand, the p42/p44 MAPK pathway activates uPA gene expression through Sp1 phosphorylation in HeLa, LNCaP and CCL39-derivative cells that do not typically express uPA in basal conditions. In HeLa cells the dominant-negative form of JNK interferes with the p42/p44 MAPK activation of the uPA-MP. The results suggest that the SAPK/JNK pathway plays an important role in the phosphorylation of Sp1, which, in turn, leads to basal or activated transcription from the uPA-MP element. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J.-Y. Chuang, Y.-T. Wang, S.-H. Yeh, Y.-W. Liu, W.-C. Chang, and J.-J. 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