Evidence map›Paper›PMID 21565933›Full record

ReviewMicrobiology (Reading, England)2011

Cytolethal distending toxin: a conserved bacterial genotoxin that blocks cell cycle progression, leading to apoptosis of a broad range of mammalian cell lineages.

Rasika N Jinadasa, Stephen E Bloom, Robert S Weiss, Gerald E Duhamel

Open access · greenAbstract readReview
In one paragraph

Review in Microbiology (Reading, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
4.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

121 citing papers in PubMed, 207 citations in OpenAlex.

  1. Review
  2. Cytolethal distending toxin enhancesInfection and immunity · 2026
    Article
  3. Review
  4. Journal of veterinary research · 2026
    Article
  5. Cytolethal Distending Toxin EnhancesbioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Review
  8. TM9SF4 acts as a receptor mediatingFrontiers in cellular and infection microbiology · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. IntratumoralPathogens (Basel, Switzerland) · 2024
    Review

61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Rasika N JinadasaDepartment of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA.
Stephen E BloomDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, USA.
Robert S WeissDepartment of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA.
Gerald E DuhamelDepartment of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA.
Cornell University · US

Funding

Contribution of Campylobacter jejuni nuclease in Animal Models of Acute InfectionR21AI085332 · NIAID · CORNELL UNIVERSITY · PI DUHAMEL, GERALD E. · 2010 to 2011
$408k
NIAID NIH HHS R21 1AI085332NIAID NIH HHS R21 AI085332
6 · The paper itself

Abstract

Cytolethal distending toxin (CDT) is a heterotrimeric AB-type genotoxin produced by several clinically important Gram-negative mucocutaneous bacterial pathogens. Irrespective of the bacterial species of origin, CDT causes characteristic and irreversible cell cycle arrest and apoptosis in a broad range of cultured mammalian cell lineages. The active subunit CdtB has structural homology with the phosphodiesterase family of enzymes including mammalian DNase I, and alone is necessary and sufficient to account for cellular toxicity. Indeed, mammalian cells treated with CDT initiate a DNA damage response similar to that elicited by ionizing radiation-induced DNA double strand breaks resulting in cell cycle arrest and apoptosis. The mechanism of CDT-induced apoptosis remains incompletely understood, but appears to involve both p53-dependent and -independent pathways. While epithelial, endothelial and fibroblast cell lines respond to CDT by undergoing arrest of cell cycle progression resulting in nuclear and cytoplasmic distension that precedes apoptotic cell death, cells of haematopoietic origin display rapid apoptosis following a brief period of cell cycle arrest. In this review, the ecology of pathogens producing CDT, the molecular biology of bacterial CDT and the molecular mechanisms of CDT-induced cytotoxicity are critically appraised. Understanding the contribution of a broadly conserved bacterial genotoxin that blocks progression of the mammalian cell cycle, ultimately causing cell death, should assist with elucidating disease mechanisms for these important pathogens.

Indexed as

ApoptosisBacterial ToxinsCell CycleDNA Breaks, Double-StrandedCell LineDeoxyribonuclease IDNA RepairGram-Negative BacteriaMutagensPhosphoric Diester HydrolasesTumor Suppressor Protein p53Bacterial Toxinscytolethal distending toxinDeoxyribonuclease IMutagensPhosphoric Diester HydrolasesTumor Suppressor Protein p53

Identifiers

PMID21565933
PMCPMC3167888
OpenAlexW2116652997

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.