ArticleTraffic (Copenhagen, Denmark)2011
Chlamydia trachomatis infection causes mitotic spindle pole defects independently from its effects on centrosome amplification.
Article in Traffic (Copenhagen, Denmark), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled 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.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Pooled it
- Inclusion Membrane Proteins ofMicroorganisms · 2026Review
- Development of a predictive model integrating urogenital pathogens and inflammatory markers for human papillomavirus infection.Frontiers in cellular and infection microbiology · 2026Article
- The Chlamydia effector Dre1 binds dynactin to reposition host organelles during infection.Cell reports · 2025Article
- Molecular Detection of Human Papillomavirus (HPV) and Other Sexually Transmitted Pathogens in Cervical and Self-Collected Specimens.International journal of molecular sciences · 2025Article
- Direct targeting of host microtubule and actin cytoskeletons by a chlamydial pathogenic effector protein.Journal of cell science · 2024Article
- The Risk of Cervical Cancer in Women Among Han, Bai, Dai and Hani Ethnic Minorities in Yunnan Province of China.International journal of women's health · 2024Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Chlamydia trachomatis IncM Protein Interferes with Host Cell Cytokinesis, Centrosome Positioning, and Golgi Distribution and Contributes to the Stability of the Pathogen-Containing Vacuole.Infection and immunity · 2023Article
- In Search of a Mechanistic Link between Chlamydia trachomatis-Induced Cellular Pathophysiology and Oncogenesis.Infection and immunity · 2023Review
- Review
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Review
- Early Transcriptional Landscapes ofFrontiers in cellular and infection microbiology · 2019Article
- The Human Centrosomal Protein CCDC146 BindsFrontiers in cellular and infection microbiology · 2018Article
- Review
- Chlamydia cell biology and pathogenesis.Nature reviews. Microbiology · 2016Review
- Conjunctival fibrosis and the innate barriers to Chlamydia trachomatis intracellular infection: a genome wide association study.Scientific reports · 2015Article
- Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections.Small GTPases · 2015Review
- Analysis of CPAF mutants: new functions, new questions (the ins and outs of a chlamydial protease).Pathogens and disease · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chlamydiae are Gram negative, obligate intracellular bacteria, and Chlamydia trachomatis is the etiologic agent of the most commonly reported sexually transmitted disease in the United States. Chlamydiae undergo a biphasic life cycle that takes place inside a parasitophorous vacuole termed an inclusion. Chlamydial infections have been epidemiologically linked to cervical cancer in patients previously infected by human papillomavirus (HPV). The inclusion associates very closely with host cell centrosomes, and this association is dependent upon the host motor protein dynein. We have previously reported that this interaction induces supernumerary centrosomes in infected cells, leading to multipolar mitotic spindles and inhibiting accurate chromosome segregation. Our findings demonstrate that chlamydial infection causes mitotic spindle defects independently of its effects on centrosome amplification. We show that chlamydial infection increases centrosome spread and inhibits the spindle assembly checkpoint delay to disrupt centrosome clustering. These data suggest that chlamydial infection exacerbates the consequences of centrosome amplification by inhibiting the cells' ability to suppress the effects of these defects on mitotic spindle organization. We hypothesize that these combined effects on mitotic spindle architecture identifies a possible mechanism for Chlamydia as a cofactor in cervical cancer formation.
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.