Evidence map›Paper›PMID 25576484›Full record

ReviewEukaryotic cell2015

DNA double-strand breaks and telomeres play important roles in trypanosoma brucei antigenic variation.

Bibo Li

Open access · diamondAbstract readReview
In one paragraph

Review in Eukaryotic cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Frontiers in cellular and infection microbiology · 2025
    Review
  3. Review
  4. Comparative Proteomic Analysis ofInternational journal of molecular sciences · 2023
    Article
  5. Telomere maintenance in African trypanosomes.Frontiers in molecular biosciences · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. DNA Double-Strand Breaks: A Double-Edged Sword for Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Bibo LiCenter for Gene Regulation in Health and Disease, Department of Biological, Geological, and Environmental Sciences, Cleveland State University, Cleveland, Ohio, USA; The Rockefeller University, New York, New York, USA; Department of Molecular Genetics, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA; Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA b.li37@csuohio.edu.
Cleveland State University · US

Funding

Mechanisms of RAP1 functions in monoallelic VSG expression in Trypanosoma bruceiR01AI066095 · NIAID · CLEVELAND STATE UNIVERSITY · PI LI, BIBO · 2007 to 2020
$5.2M
NIAID NIH HHS R01 AI066095
6 · The paper itself

Abstract

Human-infecting microbial pathogens all face a serious problem of elimination by the host immune response. Antigenic variation is an effective immune evasion mechanism where the pathogen regularly switches its major surface antigen. In many cases, the major surface antigen is encoded by genes from the same gene family, and its expression is strictly monoallelic. Among pathogens that undergo antigenic variation, Trypanosoma brucei (a kinetoplastid), which causes human African trypanosomiasis, Plasmodium falciparum (an apicomplexan), which causes malaria, Pneumocystis jirovecii (a fungus), which causes pneumonia, and Borrelia burgdorferi (a bacterium), which causes Lyme disease, also express their major surface antigens from loci next to the telomere. Except for Plasmodium, DNA recombination-mediated gene conversion is a major pathway for surface antigen switching in these pathogens. In the last decade, more sophisticated molecular and genetic tools have been developed in T. brucei, and our knowledge of functions of DNA recombination in antigenic variation has been greatly advanced. VSG is the major surface antigen in T. brucei. In subtelomeric VSG expression sites (ESs), VSG genes invariably are flanked by a long stretch of upstream 70-bp repeats. Recent studies have shown that DNA double-strand breaks (DSBs), particularly those in 70-bp repeats in the active ES, are a natural potent trigger for antigenic variation in T. brucei. In addition, telomere proteins can influence VSG switching by reducing the DSB amount at subtelomeric regions. These findings will be summarized and their implications will be discussed in this review.

Indexed as

DNA Breaks, Double-StrandedAntigens, ProtozoanTelomereTrypanosoma brucei bruceiAntigens, Protozoan

Identifiers

PMID25576484
PMCPMC4346566
OpenAlexW2156920285

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.