Repressed TGF-β signaling through CagA-Smad3 interaction as pathogenic mechanisms of Helicobacter pylori-associated gastritis
Author:
Affiliation:
1. Laboratory of Chemoprevention, Lee Gil Ya Cancer and Diabetes Institute, Gachon University
2. CHA University Cancer Prevention Research Center, CHA Bio Complex
Publisher
The Society for Free Radical Research Japan
Subject
Clinical Biochemistry,Nutrition and Dietetics,Medicine (miscellaneous)
Link
https://www.jstage.jst.go.jp/article/jcbn/57/2/57_15-38/_pdf
Reference43 articles.
1. 1 Blaser MJ, Atherton JC. Helicobacter pylori persistence: biology and disease. J Clin Invest 2004; 113: 321–333.
2. 2 Ernst PB, Crowe SE, Reyes VE. How does Helicobacter pylori cause mucosal damage? The inflammatory response. Gastroenterology 1997; 113 (6 Suppl): S35–S42; discussion S50.
3. 3 Koch M, Meyer TF, Moss SF. Inflammation, immunity, vaccines for Helicobacter pylori infection. Helicobacter 2013; 18 Suppl 1: 18–23.
4. 4 Atherton JC, Blaser MJ. Coadaptation of Helicobacter pylori and humans: ancient history, modern implications. J Clin Invest 2009; 119: 2475–2487.
5. 5 Lee JS, Paek NS, Kwon OS, Hahm KB. Anti-inflammatory actions of probiotics through activating suppressor of cytokine signaling (SOCS) expression and signaling in Helicobacter pylori infection: a novel mechanism. J Gastroenterol Hepatol 2010; 25: 194–202.
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