Evidence map›Paper›PMID 23229897›Full record

ArticleThe Journal of cell biology2012

Variant repeats are interspersed throughout the telomeres and recruit nuclear receptors in ALT cells.

Dimitri Conomos, Michael D Stutz, Mark Hills, Axel A Neumann, Tracy M Bryan, Roger R Reddel, Hilda A Pickett

Abstract read
In one paragraph

Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
–field-weighted citation impact
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

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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

101 citing papers in PubMed.

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41 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

7 authors.

Dimitri ConomosCancer Research Unit, Children's Medical Research Institute, Westmead NSW 2145, Australia.
Michael D Stutz
Mark Hills
Axel A Neumann
Tracy M Bryan
Roger R Reddel
Hilda A Pickett

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomeres in cells that use the recombination-mediated alternative lengthening of telomeres (ALT) pathway elicit a DNA damage response that is partly independent of telomere length. We therefore investigated whether ALT telomeres contain structural abnormalities that contribute to ALT activity. Here we used next generation sequencing to analyze the DNA content of ALT telomeres. We discovered that variant repeats were interspersed throughout the telomeres of ALT cells. We found that the C-type (TCAGGG) variant repeat predominated and created a high-affinity binding site for the nuclear receptors COUP-TF2 and TR4. Nuclear receptors were directly recruited to telomeres and ALT-associated characteristics were induced after incorporation of the C-type variant repeat by a mutant telomerase. We propose that the presence of variant repeats throughout ALT telomeres results from recombination-mediated telomere replication and spreading of variant repeats from the proximal regions of the telomeres and that the consequent binding of nuclear receptors alters the architecture of telomeres to facilitate further recombination.

Indexed as

Base SequenceBinding SitesCell LineCOUP Transcription Factor IIHumansMutationNuclear Receptor Subfamily 2, Group C, Member 2Protein BindingRepetitive Sequences, Nucleic AcidSequence Analysis, DNATelomeraseTelomereTelomere HomeostasisCOUP Transcription Factor IINuclear Receptor Subfamily 2, Group C, Member 2Telomerase

Identifiers

PMID23229897
PMCPMC3518223

What OpenQuestion holds

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Registered trials

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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.