ArticleScientific reports2016
Identification of E-cadherin signature motifs functioning as cleavage sites for Helicobacter pylori HtrA.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 88 citations in OpenAlex.
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- Inhibitory effects of Lactobacillus reuteri strain I300 against Helicobacter pylori adhesion, invasion, and inflammatory response in gastric epithelial cells in vitro.Folia microbiologica · 2026Article
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
- The serine protease HtrA regulates Group B Streptococcus virulence and affects the host response to infection.PLoS pathogens · 2025Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Cultivation and molecular characterization of viable Helicobacter pylori from the root canal of 170 deciduous teeth of children.Cell communication and signaling : CCS · 2024Article
- Serine protease Rv2569c facilitates transmission of Mycobacterium tuberculosis via disrupting the epithelial barrier by cleaving E-cadherin.PLoS pathogens · 2024Article
- Helicobacter pylori and Epstein-Barr virus infection in cell polarity alterations.Folia microbiologica · 2024Review
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- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Investigating the role of aFrontiers in oral health · 2024Article
- Trimer stability of Helicobacter pylori HtrA is regulated by a natural mutation in the protease domain.Medical microbiology and immunology · 2023Article
- Topical Alginate Protection against Pepsin-Mediated Esophageal Damage: E-Cadherin Proteolysis and Matrix Metalloproteinase Induction.International journal of molecular sciences · 2023Article
- Evolution and Role of Proteases inBiomolecules · 2023Review
- Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Gastric Epithelial Barrier Disruption, Inflammation and Oncogenic Signal Transduction by Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Identification of Substrates of Secreted Bacterial Protease by APEX2-Based Proximity Labeling.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Unique TLR9 Activation by Helicobacter pylori Depends on the cag T4SS, But Not on VirD2 Relaxases or VirD4 Coupling Proteins.Current microbiology · 2022Article
- E-Cadherin Orthologues as Substrates for the Serine Protease High Temperature Requirement A (HtrA).Biomolecules · 2022Article
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cell adhesion protein and tumour suppressor E-cadherin exhibits important functions in the prevention of gastric cancer. As a class-I carcinogen, Helicobacter pylori (H. pylori) has developed a unique strategy to interfere with E-cadherin functions. In previous studies, we have demonstrated that H. pylori secretes the protease high temperature requirement A (HtrA) which cleaves off the E-cadherin ectodomain (NTF) on epithelial cells. This opens cell-to-cell junctions, allowing bacterial transmigration across the polarised epithelium. Here, we investigated the molecular mechanism of the HtrA-E-cadherin interaction and identified E-cadherin cleavage sites for HtrA. Mass-spectrometry-based proteomics and Edman degradation revealed three signature motifs containing the [VITA]-[VITA]-x-x-D-[DN] sequence pattern, which were preferentially cleaved by HtrA. Based on these sites, we developed a substrate-derived peptide inhibitor that selectively bound and inhibited HtrA, thereby blocking transmigration of H. pylori. The discovery of HtrA-targeted signature sites might further explain why we detected a stable 90 kDa NTF fragment during H. pylori infection, but also additional E-cadherin fragments ranging from 105 kDa to 48 kDa in in vitro cleavage experiments. In conclusion, HtrA targets E-cadherin signature sites that are accessible in in vitro reactions, but might be partially masked on epithelial cells through functional homophilic E-cadherin interactions.
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