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    Helicobacter pylori stimulates host cyclooxygenase-2 gene transcription: critical importance of MEK/ERK-dependent activation of USF1/-2 and CREB transcription factors.

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    Author
    Jüttner, S; Cramer, T; Wessler, S; Walduck, A; Gao, F; Schmitz, F; Wunder, C; Weber, M; Fischer, SM; Schmidt, WE; ...
    Date
    2003-11
    Source Title
    Cellular Microbiology
    Publisher
    Wiley
    University of Melbourne Author/s
    WALDUCK, ANNA
    Affiliation
    Microbiology And Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Jüttner, S., Cramer, T., Wessler, S., Walduck, A., Gao, F., Schmitz, F., Wunder, C., Weber, M., Fischer, S. M., Schmidt, W. E., Wiedenmann, B., Meyer, T. F., Naumann, M. & Höcker, M. (2003). Helicobacter pylori stimulates host cyclooxygenase-2 gene transcription: critical importance of MEK/ERK-dependent activation of USF1/-2 and CREB transcription factors.. Cell Microbiol, 5 (11), pp.821-834. https://doi.org/10.1046/j.1462-5822.2003.00324.x.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/26629
    DOI
    10.1046/j.1462-5822.2003.00324.x
    Description

    C1 - Journal Articles Refereed

    Abstract
    Cyclooxygenase-2 (COX-2) represents the inducible key enzyme of arachidonic acid metabolism and contributes to the pathogenesis of gastroduodenal ulcers and gastric cancer. Helicobacter pylori infection is associated with elevated gastric COX-2 levels, but the mechanisms underlying H. pylori-dependent cox-2 gene expression are unclear. H. pylori stimulated cox-2 mRNA and protein abundance in gastric epithelial cells in vitro and in vivo, and functional analysis of the cox-2 gene promoter mapped its H. pylori-responsive region to a proximal CRE/Ebox element at -56 to -48. Moreover, USF1/-2 and CREB transcription factors binding to this site were identified to transmit H. pylori-dependent cox-2 transcription. Activation of MEK/ERK1/-2 signalling by bacterial virulence factors located outside the H. pylori cag pathogenicity island (cagPAI) was found to mediate bacterial effects on the cox-2 promoter. Our study provides a detailed description of the molecular pathways underlying H. pylori-dependent cox-2 gene expression in gastric epithelial cells, and may thus contribute to a better understanding of mechanisms underlying H. pylori pathogenicity.
    Keywords
    Bacteriology ; Infectious Diseases; Infectious Diseases

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