Extracellular signal-regulated kinase induces phosphorylation of IκBα in Helicobacter pylori-infected gastric epithelial AGS cells

S. O. Cho, K. H. Kim, H. Kim

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-κB regulates the expression of inflammatory genes. NF-κB is activated by phsophorylation of its endogenous inhibitor, IκBα. The possible involvement of mitogenactivated protein kinase (MAPK) on NF-κB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkBα and whether H. pylori-induced phosphorylation of IkBα 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 IκBα accompanied with the decrease in control IκBα. H. pylori-induced phosphorylation of IκBα was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IκBα in H. pylori-infected AGS cells.

Original languageEnglish
Pages (from-to)26-30
Number of pages5
JournalInflammopharmacology
Volume15
Issue number1
DOIs
Publication statusPublished - 2007 Feb 1

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Extracellular Signal-Regulated MAP Kinases
Helicobacter pylori
Stomach
Epithelial Cells
Phosphorylation
Protein Kinases
JNK Mitogen-Activated Protein Kinases
Protein Kinase Inhibitors
Phosphotransferases
Gene Expression

All Science Journal Classification (ASJC) codes

  • Immunology
  • Pharmacology
  • Pharmacology (medical)

Cite this

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title = "Extracellular signal-regulated kinase induces phosphorylation of IκBα in Helicobacter pylori-infected gastric epithelial AGS cells",
abstract = "In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-κB regulates the expression of inflammatory genes. NF-κB is activated by phsophorylation of its endogenous inhibitor, IκBα. The possible involvement of mitogenactivated protein kinase (MAPK) on NF-κB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkBα and whether H. pylori-induced phosphorylation of IkBα 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 IκBα accompanied with the decrease in control IκBα. H. pylori-induced phosphorylation of IκBα was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IκBα in H. pylori-infected AGS cells.",
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Extracellular signal-regulated kinase induces phosphorylation of IκBα in Helicobacter pylori-infected gastric epithelial AGS cells. / Cho, S. O.; Kim, K. H.; Kim, H.

In: Inflammopharmacology, Vol. 15, No. 1, 01.02.2007, p. 26-30.

Research output: Contribution to journalArticle

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