Evidence map›Paper›PMID 10811624›Full record

ArticleThe EMBO journal2000

Telomere maintenance and length regulation in Trypanosoma brucei.

D Horn, C Spence, A K Ingram

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Microbiology spectrum · 2026
    Article
  2. Article
  3. Article
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  6. VEX1 controls the allelic exclusion required for antigenic variation in trypanosomes.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  7. Review
  8. Article
  9. Article
  10. Telomere length in Trypanosoma brucei.Experimental parasitology · 2008
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The central roles of telomeres and subtelomeres in antigenic variation in African trypanosomes.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2005
    Review
  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

3 authors at 1 institution in 1 country.

D HornLondon School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, UK. david.horn@lshtm.ac.uk.
C Spence
A K Ingram
London School of Hygiene & Tropical Medicine · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Transcription of telomere proximal variant surface glycoprotein genes is mono-allelic in bloodstream-form Trypanosoma brucei. The terminal DNA sequence at these telomeres consists of tandem T(2)AG(3) repeats, which increase in length by approximately 8 bp per cell division balanced by occasional loss of large numbers of repeats. Here we have used targeted chromosome fragmentation to investigate the sequence requirements for telomere formation in T. brucei. Telomere formation is most efficient on tandem T(2)AG(3) repeats, but can also occur on specific templates found within 'random' sequence substrates and on G-rich motifs proximal to a double-strand break. Newly formed telomeres are extended faster than other native telomeres, but as the telomere becomes longer the rate of extension declines. Telomere length regulation in T.brucei is discussed in the context of recent results from other cell types.

Indexed as

AnimalsTelomeraseTelomereTranscription, GeneticTrypanosoma brucei bruceiTelomerase

Identifiers

PMID10811624
PMCPMC384376
OpenAlexW2088086955

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.