ArticleOncogene1999
The bacterial cytolethal distending toxin (CDT) triggers a G2 cell cycle checkpoint in mammalian cells without preliminary induction of DNA strand breaks.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 74 citations in OpenAlex.
- Article
- Article
- Cytolethal Distending Toxin Promotes Replicative Stress Leading to Genetic Instability Transmitted to Daughter Cells.Frontiers in cell and developmental biology · 2021Article
- Genotoxic Effect ofmBio · 2020Article
- Bacterial Genotoxin-Induced DNA Damage and Modulation of the Host Immune Microenvironment.Toxins · 2020Review
- Prophylactic potential of cytolethal distending toxin B (CdtB) subunit of typhoid toxin against Typhoid fever.Scientific reports · 2019Article
- Ciclopirox inhibits cancer cell proliferation by suppression of Cdc25A.Genes & cancer · 2017Article
- Haemophilus parasuis cytolethal distending toxin induces cell cycle arrest and p53-dependent apoptosis.PloS one · 2017Article
- Genomic Comparison of Campylobacter spp. and Their Potential for Zoonotic Transmission between Birds, Primates, and Livestock.Applied and environmental microbiology · 2016Article
- Review
- The Cytolethal Distending Toxin Contributes to Microbial Virulence and Disease Pathogenesis by Acting As a Tri-Perditious Toxin.Frontiers in cellular and infection microbiology · 2016Review
- Review
- Distinct Roles for CdtA and CdtC during Intoxication by Cytolethal Distending Toxins.PloS one · 2015Article
- Article
- Prevalence and pathogenic potential of campylobacter isolates from free-living, human-commensal american crows.Applied and environmental microbiology · 2014Article
- High prevalence of mucosa-associated E. coli producing cyclomodulin and genotoxin in colon cancer.PloS one · 2013Article
- Bacterial toxin modulation of the eukaryotic cell cycle: are all cytolethal distending toxins created equally?Frontiers in cellular and infection microbiology · 2012Review
- The biology of the cytolethal distending toxins.Toxins · 2011Review
- The struggle within: microbial influences on colorectal cancer.Inflammatory bowel diseases · 2011Review
- Bacterial intoxication evokes cellular senescence with persistent DNA damage and cytokine signalling.Journal of cellular and molecular medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bacterial cytolethal distending toxin (CDT) was previously shown to arrest the tumor-derived HeLa cell line in the G2-phase of the cell cycle through inactivation of CDK1, a cyclin-dependent kinase whose state of activation determines entry into mitosis. We have analysed the effects induced in HeLa cells by CDT, in comparison to those induced by etoposide, a prototype anti-tumoral agent that triggers a G2 cell cycle checkpoint by inducing DNA damage. Both CDT and etoposide inhibit cell proliferation and induces the formation of enlarged mononucleated cells blocked in G2. In both cases, CDK1 from arrested cells could be reactivated both in vitro by dephosphorylation by recombinant Cdc25B phosphatase and in vivo by caffeine. However, the cell cycle arrest triggered by CDT, unlike etoposide, did not originate from DNA strand breaks as demonstrated in the single cell gel electrophoresis assay and by the absence of slowing down of S phase in synchronized cells. Together with additional observations on synchronized HeLa cells, our results suggest that CDT triggers a G2 cell cycle checkpoint that is initiated during DNA replication and that is independent of DNA damage.
Indexed as
Identifiers
What OpenQuestion holds
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.