ArticleCell communication and signaling : CCS2019
Helicobacter pylori-controlled c-Abl localization promotes cell migration and limits apoptosis.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting ferroptosis inInternational journal of oncology · 2026Review
- Infection and herbicide exposure implicate c-Abl kinase in α-Synuclein Ser129 phosphorylation.Cell communication and signaling : CCS · 2025Article
- Programmed cell death inFrontiers in cellular and infection microbiology · 2024Review
- Review
- Unwelcome guests - the role of gland-associatedFrontiers in oncology · 2023Review
- Global Trend on Machine Learning inGlobal health, epidemiology and genomics · 2023Article
- Gastric Epithelial Barrier Disruption, Inflammation and Oncogenic Signal Transduction by Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Chronic inflammation and long-lasting changes in the gastric mucosa after Helicobacter pylori infection involved in gastric cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Article
- Gastric Cancer: Advances in Carcinogenesis Research and New Therapeutic Strategies.International journal of molecular sciences · 2021Review
- TAZ ControlsCells · 2020Article
- Sustained Exposure toFrontiers in oncology · 2020Article
- Tyrosine Kinases inToxins · 2019Review
- Review: Pathogenesis of Helicobacter pylori infection.Helicobacter · 2019Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundDeregulated c-Abl activity has been intensively studied in a variety of solid tumors and leukemia. The class-I carcinogen Helicobacter pylori (Hp) activates the non-receptor tyrosine kinase c-Abl to phosphorylate the oncoprotein cytotoxin-associated gene A (CagA). The role of c-Abl in CagA-dependent pathways is well established; however, the knowledge of CagA-independent c-Abl processes is scarce.
methodsc-Abl phosphorylation and localization were analyzed by immunostaining and immunofluorescence. Interaction partners were identified by tandem-affinity purification. Cell elongation and migration were analyzed in transwell-filter experiments. Apoptosis and cell survival were examined by FACS analyses and MTT assays. In mice experiments and human biopsies, the involvement of c-Abl in Hp pathogenesis was investigated.
resultsHere, we investigated the activity and subcellular localization of c-Abl in vitro and in vivo and unraveled the contribution of c-Abl in CagA-dependent and -independent pathways to gastric Hp pathogenesis. We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAbl
conclusionsIn this study, we identified a novel regulatory mechanism in Hp-infected gastric epithelial cells by which Hp determines the subcellular localization of activated c-Abl to control Hp-mediated EMT-like processes while decreasing cell death.
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