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  • Title: Extracellular signal-regulated kinase induces phosphorylation of IkappaBalpha in Helicobacter pylori-infected gastric epithelial AGS cells.
    Author: Cho SO, Kim KH, Kim H.
    Journal: Inflammopharmacology; 2007 Feb; 15(1):26-30. PubMed ID: 17323192.
    Abstract:
    In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-kappaB regulates the expression of inflammatory genes. NF-kappaB is activated by phosphorylation of its endogenous inhibitor, IkappaBalpha. The possible involvement of mitogen-activated protein kinase (MAPK) on NF-kappaB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkappaBalpha and whether H. pylori-induced phosphorylation of IkappaBalpha is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IkappaBalpha accompanied with the decrease in control IkappaBalpha. H. pylori-induced phosphorylation of IkappaBalpha was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IkappaBalpha in H. pylori-infected AGS cells.
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