TY  - JOUR
AU  - Jüttner, S
AU  - Cramer, T
AU  - Wessler, S
AU  - Walduck, A
AU  - Gao, F
AU  - Schmitz, F
AU  - Wunder, C
AU  - Weber, M
AU  - Fischer, SM
AU  - Schmidt, WE
AU  - Wiedenmann, B
AU  - Meyer, TF
AU  - Naumann, M
AU  - Höcker, M
Y2  - 2014/05/21
Y1  - 2003/11
SN  - 1462-5814
UR  - http://hdl.handle.net/11343/26629
AB  - 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.
N1  - application/pdf
LA  - eng
PB  - Wiley
KW  - Bacteriology ; Infectious Diseases; Infectious Diseases
T1  - Helicobacter pylori stimulates host cyclooxygenase-2 gene transcription: critical importance of MEK/ERK-dependent activation of USF1/-2 and CREB transcription factors.
DO  - 10.1046/j.1462-5822.2003.00324.x
IS  - Cellular Microbiology
VL  - 5
IS  - 11
SP  - 821-834
L1  - /bitstream/handle/11343/26629/116849_5483.pdf?sequence=1&isAllowed=n
ER  -