ArticlePLoS pathogens2016
Regulation of Rac1 and Reactive Oxygen Species Production in Response to Infection of Gastrointestinal Epithelia.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Apurinic/apyrimidinic endonuclease 1 prevents oxidative DNA damage in intestinal epithelial cells induced by genotoxic Escherichia coli NC101.Redox biology · 2026Article
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Choroid plexus organoids reveal mechanisms of Streptococcus suis translocation at the blood-cerebrospinal fluid barrier.Fluids and barriers of the CNS · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Alterations in Adipose Tissue and Adipokines in Heterozygous APE1/Ref-1 Deficient Mice.Endocrinology and metabolism (Seoul, Korea) · 2024Article
- Apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) promotes stress granule formation via YBX1 phosphorylation in ovarian cancer.Cellular and molecular life sciences : CMLS · 2024Article
- The crosstalk between microbial sensors ELMO1 and NOD2 shape intestinal immune responses.Virulence · 2023Article
- Isotope tracing reveals bacterial catabolism of host-derived glutathione during Helicobacter pylori infection.PLoS pathogens · 2023Article
- Rac1 inhibition protects the kidney against kidney ischemia/reperfusion through the inhibition of macrophage migration.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Prognostic biomarkers and molecular pathways mediating Helicobacter pylori-induced gastric cancer: a network-biology approach.Genomics & informatics · 2023Article
- Bacterial infection and microbiota in carcinogenesis and tumor development.Frontiers in cellular and infection microbiology · 2023Review
- A Novel HypomorphicAntioxidants & redox signaling · 2023Article
- SIRT1/APE1 promotes the viability of gastric cancer cells by inhibiting p53 to suppress ferroptosis.Open medicine (Warsaw, Poland) · 2023Article
- Organoid-on-a-chip model of human ARPKD reveals mechanosensing pathomechanisms for drug discovery.Science advances · 2022Article
- Comparison of Selenium-EnrichedNutrients · 2022Article
- Antibacterial Effects of Bacteriocin PLNC8 againstFoods (Basel, Switzerland) · 2022Article
- APE1/Ref-1 Role in Inflammation and Immune Response.Frontiers in immunology · 2022Review
- Potential Role of APEX1 During Ferroptosis.Frontiers in oncology · 2022Review
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Generation of reactive oxygen species (ROS) during infection is an immediate host defense leading to microbial killing. APE1 is a multifunctional protein induced by ROS and after induction, protects against ROS-mediated DNA damage. Rac1 and NAPDH oxidase (Nox1) are important contributors of ROS generation following infection and associated with gastrointestinal epithelial injury. The purpose of this study was to determine if APE1 regulates the function of Rac1 and Nox1 during oxidative stress. Gastric or colonic epithelial cells (wild-type or with suppressed APE1) were infected with Helicobacter pylori or Salmonella enterica and assessed for Rac1 and NADPH oxidase-dependent superoxide production. Rac1 and APE1 interactions were measured by co-immunoprecipitation, confocal microscopy and proximity ligation assay (PLA) in cell lines or in biopsy specimens. Significantly greater levels of ROS were produced by APE1-deficient human gastric and colonic cell lines and primary gastric epithelial cells compared to control cells after infection with either gastric or enteric pathogens. H. pylori activated Rac1 and Nox1 in all cell types, but activation was higher in APE1 suppressed cells. APE1 overexpression decreased H. pylori-induced ROS generation, Rac1 activation, and Nox1 expression. We determined that the effects of APE1 were mediated through its N-terminal lysine residues interacting with Rac1, leading to inhibition of Nox1 expression and ROS generation. APE1 is a negative regulator of oxidative stress in the gastrointestinal epithelium during bacterial infection by modulating Rac1 and Nox1. Our results implicate APE1 in novel molecular interactions that regulate early stress responses elicited by microbial infections.
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