ArticleOncogene2007
Phosphorylation of Helicobacter pylori CagA by c-Abl leads to cell motility.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
93 citing papers in PubMed, 175 citations in OpenAlex.
- Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model.International journal of molecular sciences · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Infection and herbicide exposure implicate c-Abl kinase in α-Synuclein Ser129 phosphorylation.Cell communication and signaling : CCS · 2025Article
- Microbial molecules, metabolites, and malignancy.Neoplasia (New York, N.Y.) · 2025Review
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Research progress on the impact and mechanisms of helicobacter pylori infection on the efficacy of immunotherapy for gastric cancer.Frontiers in oncology · 2025Review
- T4SEpp: A pipeline integrating protein language models to predict bacterial type IV secreted effectors.Computational and structural biotechnology journal · 2024Article
- HtrA-Dependent E-Cadherin Shedding Impairs the Epithelial Barrier Function in Primary Gastric Epithelial Cells and Gastric Organoids.International journal of molecular sciences · 2024Article
- Immune evasion by proteolytic shedding of natural killer group 2, member D ligands inFrontiers in immunology · 2024Article
- Implications of silver nanoparticles forFrontiers in cellular and infection microbiology · 2024Article
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Intersections between innate immune response and gastric cancer development.World journal of gastroenterology · 2023Review
- Review
- New CagL Amino Acid Polymorphism Patterns ofMedicina (Kaunas, Lithuania) · 2022Article
- Influence ofWorld journal of clinical oncology · 2022Review
- Role of nickel-regulated small RNA in modulation ofWorld journal of clinical cases · 2022Review
- Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Review
- Article
- Cortactin Is Required for Efficient FAK, Src and Abl Tyrosine Kinase Activation and Phosphorylation ofInternational journal of molecular sciences · 2021Article
- Exploring the Distinct Binding and Activation Mechanisms for Different CagA Oncoproteins and SHP2 by Molecular Dynamics Simulations.Molecules (Basel, Switzerland) · 2021Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori induces a strong motogenic response in infected gastric epithelial host cells, which is enhanced by translocation of the pathogenic factor cytotoxin-associated gene A (CagA) into host cells via a specialized type IV secretion system. Once injected into the cytosol CagA is rapidly tyrosine phosphorylated by Src family kinases followed by Src inactivation. Hence, it remained unknown why CagA is constantly phosphorylated in sustained H. pylori infections to induce cell migration, whereas other substrates of Src kinases are dephosphorylated. Here, we identify the non-receptor tyrosine kinase c-Abl as a crucial mediator of H. pylori-induced migration and novel CagA kinase in epithelial cells. Upon H. pylori infection c-Abl directly interacts with CagA and localizes in focal adhesion complexes and membrane ruffles, which are highly dynamic cytoskeletal structures necessary for cell motility. Selective inhibition of c-Abl kinase activity by STI571 or shRNA abrogates sustained CagA phosphorylation and epithelial cell migration, indicating a pivotal role of c-Abl in H. pylori infection and pathogenicity. These results implicate c-Abl as a novel molecular target for therapeutic intervention in H. pylori-related gastric diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.