Evidence map›Paper›PMID 32620872›Full record

ArticleNature communications2020

Persistent telomere cohesion protects aged cells from premature senescence.

Kameron Azarm, Amit Bhardwaj, Eugenie Kim, Susan Smith

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  8. Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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  16. Article
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  19. Review
  20. Nuclear PARPs and genome integrity.Genes & development · 2020
    Review
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.

Kameron AzarmKimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
Amit BhardwajKimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.
Eugenie KimKimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA.ORCID http://orcid.org/0000-0003-4619-2653
Susan SmithKimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, NY, 10016, USA. susan.smith@med.nyu.edu.ORCID http://orcid.org/0000-0002-8213-5915
New York University · US

Funding

Regulation of telomere recombination in ALT cancer cellsR01CA200751 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SMITH, SUSAN · 2016 to 2020
$2.0M
Understanding the role of persistent telomere cohesion in ALT cancer cellsF31CA221162 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI AZARM, KAMERON · 2018 to 2020
$80k
NCI NIH HHS F31 CA221162NCI NIH HHS R01 CA200751
6 · The paper itself

Abstract

Human telomeres are bound by the telomere repeat binding proteins TRF1 and TRF2. Telomere shortening in human cells leads to a DNA damage response that signals replicative senescence. While insufficient loading of TRF2 at shortened telomeres contributes to the DNA damage response in senescence, the contribution of TRF1 to senescence induction has not been determined. Here we show that counter to TRF2 deficiency-mediated induction of DNA damage, TRF1 deficiency serves a protective role to limit induction of DNA damage induced by subtelomere recombination. Shortened telomeres recruit insufficient TRF1 and as a consequence inadequate tankyrase 1 to resolve sister telomere cohesion. Our findings suggest that the persistent cohesion protects short telomeres from inappropriate recombination. Ultimately, in the final division, telomeres are no longer able to maintain cohesion and subtelomere copying ensues. Thus, the gradual loss of TRF1 and concomitant persistent cohesion that occurs with telomere shortening ensures a measured approach to replicative senescence.

Indexed as

Base SequenceCell LineCell Line, TumorCellular SenescenceDNA DamageHEK293 CellsHeterochromatinHumansIn Situ Hybridization, FluorescenceMutationRNA InterferenceTankyrasesTelomereTelomere ShorteningTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 2HeterochromatinTankyrasesTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 2TERF2 protein, human

Identifiers

PMID32620872
PMCPMC7335080
OpenAlexW3038649739

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.