ArticleScientific reports2019
Increased LIGHT expression and activation of non-canonical NF-κB are observed in gastric lesions of MyD88-deficient mice upon Helicobacter felis infection.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular surveillance ofOne health (Amsterdam, Netherlands) · 2024Article
- TRIF-IFN-I pathway iniScience · 2024Article
- GRB7 plays a promoting role in the progression of gastric cancer.BMC cancer · 2023Article
- Genomically Silent Refractory Gastric Cancer in a Young Patient Exhibits Overexpression of CXCL5.Current oncology (Toronto, Ont.) · 2022Article
- Engagement of CEACAM1 byMicroorganisms · 2021Article
- LncRNA HOXA-AS3 promotes gastric cancer progression by regulating miR-29a-3p/LTβR and activating NF-κB signaling.Cancer cell international · 2021Article
- Microbiome Signatures in a Fast- and Slow-Progressing Gastric Cancer Murine Model and Their Contribution to Gastric Carcinogenesis.Microorganisms · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
Helicobacter pylori infection induces a number of pro-inflammatory signaling pathways contributing to gastric inflammation and carcinogenesis. Among those, NF-κB signaling plays a pivotal role during infection and malignant transformation of the gastric epithelium. However, deficiency of the adaptor molecule myeloid differentiation primary response 88 (MyD88), which signals through NF-κB, led to an accelerated development of gastric pathology upon H. felis infection, but the mechanisms leading to this phenotype remained elusive. Non-canonical NF-κB signaling was shown to aggravate H. pylori-induced gastric inflammation via activation of the lymphotoxin β receptor (LTβR). In the present study, we explored whether the exacerbated pathology observed in MyD88-deficient (Myd88
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