ArticleNature communications2020
The ALPK1/TIFA/NF-κB axis links a bacterial carcinogen to R-loop-induced replication stress.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Identification of microbial markers across populations in early detection of colorectal cancer.Nature communications · 2021Pooled it
- Host andGut microbes · 2026Article
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Stromal BMP signalling maintains stem cell genome integrity and prevents gastric cancer initiation.Cell death & disease · 2026Article
- Drugging non-canonical kinases in cancer therapeutics: Molecular targets, underlying mechanisms and small-molecule inhibitors.Acta pharmaceutica Sinica. B · 2026Review
- Fusobacterium nucleatum in oral squamous cell carcinoma: molecular mechanisms, tumor microenvironment and translational implications.Archives of microbiology · 2026Review
- Distinct mechanisms of replication stress induced by oncogenic RAS and cyclin E1 converge on R-loop-dependent fork reversal.Nature communications · 2026Article
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- TIFA: a signaling hub linking inflammation, innate immunity, and human disease.Frontiers in immunology · 2026Review
- Comparative effectiveness of genotype-guided and empirical bismuth-containing quadruple therapy forFrontiers in pharmacology · 2026Article
- Research Status and Prospects ofGastroenterology research and practice · 2026Review
- Extracts from Plectranthus asirensis and Premna resinosa inhibit Helicobacter pylori-induced epithelial cell damage, DNA double-strand breaks and inflammation.Gut pathogens · 2025Article
- Molecular characterization of fourGut microbes · 2025Article
- Roles of the lipopolysaccharide biosynthesis-related geneVirulence · 2025Article
- The importance of ALPK1 kinase functionality as a potential biomarker for inflammatory diseases.Molecular biology reports · 2025Review
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- Enhanced LRP8 expression induced by Helicobacter pylori drives gastric cancer progression by facilitating β-Catenin nuclear translocation.Journal of advanced research · 2025Article
- Article
- Advances in Helicobacter pylori lipopolysaccharide structure and function.FEMS microbiology reviews · 2025Review
7 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
20 authors at 7 institutions in 5 countries.
Funding
Abstract
Exposure of gastric epithelial cells to the bacterial carcinogen Helicobacter pylori causes DNA double strand breaks. Here, we show that H. pylori-induced DNA damage occurs co-transcriptionally in S-phase cells that activate NF-κB signaling upon innate immune recognition of the lipopolysaccharide biosynthetic intermediate β-ADP-heptose by the ALPK1/TIFA signaling pathway. DNA damage depends on the bi-functional RfaE enzyme and the Cag pathogenicity island of H. pylori, is accompanied by replication fork stalling and can be observed also in primary cells derived from gastric organoids. Importantly, H. pylori-induced replication stress and DNA damage depend on the presence of co-transcriptional RNA/DNA hybrids (R-loops) that form in infected cells during S-phase as a consequence of β-ADP-heptose/ ALPK1/TIFA/NF-κB signaling. H. pylori resides in close proximity to S-phase cells in the gastric mucosa of gastritis patients. Taken together, our results link bacterial infection and NF-κB-driven innate immune responses to R-loop-dependent replication stress and DNA damage.
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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.