ArticleInfection and immunity2014
Role of connexin 43 in Helicobacter pylori VacA-induced cell death.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- The Expression Analysis ofInternational journal of hematology-oncology and stem cell research · 2024Article
- Emerging role of human microbiome in cancer development and response to therapy: special focus on intestinal microflora.Journal of translational medicine · 2022Review
- How doesWorld journal of gastroenterology · 2019Review
- Prognostic value of the mRNA expression of gap junction α members in patients with gastric cancer.Oncology letters · 2019Article
- An improved method for increasing the efficiency of gene transfection and transduction.International journal of physiology, pathophysiology and pharmacology · 2018Article
- Helicobacter pylori VacA induces autophagic cell death in gastric epithelial cells via the endoplasmic reticulum stress pathway.Cell death & disease · 2017Article
- Review
- Strategies used byWorld journal of gastroenterology · 2017Review
- Helicobacter pylori as an oncogenic pathogen, revisited.Expert reviews in molecular medicine · 2017Review
- Helicobacter pylori VacA, acting through receptor protein tyrosine phosphatase α, is crucial for CagA phosphorylation in human duodenum carcinoma cell line AZ-521.Disease models & mechanisms · 2016Article
- Systems Biology-Based Investigation of Cellular Antiviral Drug Targets Identified by Gene-Trap Insertional Mutagenesis.PLoS computational biology · 2016Article
- A Nonoligomerizing Mutant Form of Helicobacter pylori VacA Allows Structural Analysis of the p33 Domain.Infection and immunity · 2016Article
- Cytoplasmic vacuolization in cell death and survival.Oncotarget · 2016Review
- Review
- Review
- Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori.Current opinion in infectious diseases · 2016Review
- Connexin and pannexin signaling in gastrointestinal and liver disease.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Pathogenesis of Helicobacter pylori Infection.Helicobacter · 2015Review
- Helicobacter pylori VacA induces apoptosis by accumulation of connexin 43 in autophagic vesicles via a Rac1/ERK-dependent pathway.Cell death discovery · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Helicobacter pylori colonizes the human stomach and confers an increased risk for the development of peptic ulceration, noncardia gastric adenocarcinoma, and gastric lymphoma. A secreted H. pylori toxin, VacA, can cause multiple alterations in gastric epithelial cells, including cell death. In this study, we sought to identify host cell factors that are required for VacA-induced cell death. To do this, we analyzed gene trap and short hairpin RNA (shRNA) libraries in AZ-521 human gastric epithelial cells and selected for VacA-resistant clones. Among the VacA-resistant clones, we identified multiple gene trap library clones and an shRNA library clone with disrupted expression of connexin 43 (Cx43) (also known as gap junction protein alpha 1 [GJA1]). Further experiments with Cx43-specific shRNAs confirmed that a reduction in Cx43 expression results in resistance to VacA-induced cell death. Immunofluorescence microscopy experiments indicated that VacA did not colocalize with Cx43. We detected production of the Cx43 protein in AZ-521 cells but not in AGS, HeLa, or RK-13 cells, and correspondingly, AZ-521 cells were the most susceptible to VacA-induced cell death. When Cx43 was expressed in HeLa cells, the cells became more susceptible to VacA. These results indicate that Cx43 is a host cell constituent that contributes to VacA-induced cell death and that variation among cell types in susceptibility to VacA-induced cell death is attributable at least in part to cell type-specific differences in Cx43 production.
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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.