ArticleJournal of cancer prevention2013
Differential Role of ERK and p38 on NF- κ B Activation in Helicobacter pylori-Infected Gastric Epithelial Cells.
Article in Journal of cancer prevention, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Impairment of neuronal tyrosine phosphatase STEP worsens post-ischemic inflammation and brain injury under hypertensive condition.Journal of neuroinflammation · 2024Article
- The Tryptophan Metabolite Indole-3-Carboxaldehyde Alleviates Mice with DSS-Induced Ulcerative Colitis by Balancing Amino Acid Metabolism, Inhibiting Intestinal Inflammation, and Improving Intestinal Barrier Function.Molecules (Basel, Switzerland) · 2023Article
- PARP2 downregulation in T cells ameliorates lipopolysaccharide-induced inflammation of the large intestine.Frontiers in immunology · 2023Article
- The Role of Formyl Peptide Receptors in Permanent and Low-Grade Inflammation:International journal of molecular sciences · 2021Review
- New approach of medicinal herbs and sulfasalazine mixture on ulcerative colitis induced by dextran sodium sulfate.World journal of gastroenterology · 2020Article
- MAP Kinases Pathways in Gastric Cancer.International journal of molecular sciences · 2020Review
- Extracellular HMGB-1 activates inflammatory signaling in tendon cells and tissues.Therapeutic advances in chronic disease · 2020Article
- Lactobacillus paracasei strain 06TCa19 suppresses inflammatory chemokine induced by Helicobacter pylori in human gastric epithelial cells.Human cell · 2017Article
- Comparative Evaluation between Sulfasalazine Alone and in Combination with Herbal Medicine on DSS-Induced Ulcerative Colitis Mice.BioMed research international · 2017Article
- Banhasasim-Tang Treatment Reduces the Severity of Esophageal Mucosal Ulcer on Chronic Acid Reflux Esophagitis in Rats.BioMed research international · 2017Article
- Petri Net-Based Model ofFrontiers in microbiology · 2017Article
- Effect ofExperimental and therapeutic medicine · 2016Article
- Safflower Yellow regulates microglial polarization and inhibits inflammatory response in LPS-stimulated Bv2 cells.International journal of immunopathology and pharmacology · 2016Article
- Protective effect of Rhei Rhizoma on reflux esophagitis in rats via Nrf2-mediated inhibition of NF-κB signaling pathway.BMC complementary and alternative medicine · 2016Article
- Trefoil factor 1 expression suppresses Helicobacter pylori-induced inflammation in gastric carcinogenesis.Cancer · 2015Article
- Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.Journal of translational medicine · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF- κ B in gastric epithelial cells. Mitogen-activated protein kinases including extracellular signal-regulated kinase (ERK) and p38 kinase (p38) are activated by Helicobacter pylori, which may regulate NF- κ B activation in the infected cells. However the mechanisms how ERK and p38 induce NF- κ B activation have not been investigated. Present study aims to investigate the role of ERK and p38 on the activation of NF- κ B in Helicobacter pylori-infected AGS cells. Western blot analysis was performed for determining the levels of I κ B, p105, p50 and p65 in gastric epithelial cells infected with Helicobacter pylori and treated with ERK inhibitor U0126 and p38 inhibitor SB203580. Helicobacter pylori induced the degradation of I κ Bα and upregulation of p105, p50 and p65 in the infected cells. U0126 inhibited the degradation of I κ Bα while SB203580 suppressed expression of p105, p50 and p65 in Helicobacter pylori-infected cells. ERK and p38 differentially activate NF- κ B; ERK induces degradation of I κ Bα while p38 upregulates the expression of p50 and p65, subunits of NF-κB in Helicobacter pylori-infected gastric epithelial AGS cells.
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