Evidence map›Paper›PMID 26941064›Full record

ArticleNature communications2016

TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions.

Rekha Rai, Yong Chen, Ming Lei, Sandy Chang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 134 citations in OpenAlex.

  1. Abnormal mRNA Expression Levels of Telomere-Binding Proteins Represent Biomarkers in Myelodysplastic Syndromes: A Case-Control Study.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2017
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  4. 3,6'-Disinapoyl Sucrose fromAntioxidants (Basel, Switzerland) · 2026
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  16. Article
  17. Telomere Elongation During Pre-Implantation Embryo Development.Advances in anatomy, embryology, and cell biology · 2024
    Review
  18. Review
  19. Article
  20. Review

36 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

4 authors at 2 institutions in 2 countries.

Rekha RaiDepartment of Laboratory Medicine, Yale University School of Medicine, 330 Cedar Street, New Haven, Connecticut 06520, USA.
Yong ChenNational Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences 333, Haike Rd., Shanghai 201210, China.
Ming LeiNational Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences 333, Haike Rd., Shanghai 201210, China.
Sandy ChangDepartment of Laboratory Medicine, Yale University School of Medicine, 330 Cedar Street, New Haven, Connecticut 06520, USA.
Center for Excellence in Molecular Cell Science · CNYale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
Telomere induced senescence as a supressor of tumorigenesisR01CA129037 · NCI · YALE UNIVERSITY · PI CHANG, SANDY S · 2007 to 2017
$3.1M
Telomere dysfunction induced breast cancer pathogenesisR01CA202816 · NCI · YALE UNIVERSITY · PI CHANG, SANDY S · 2016 to 2020
$1.9M
Telomere replication and maintenance of genome stabilityR21AG043747 · NIA · YALE UNIVERSITY · PI CHANG, SANDY S · 2013 to 2014
$458k
Telomere dysfunction and genome instability in familial melanomaR21CA200506 · NCI · YALE UNIVERSITY · PI CHANG, SANDY S · 2016 to 2017
$400k
Understanding alternative non-homologous end joining repair in telomere dysfunctiR21CA182280 · NCI · YALE UNIVERSITY · PI CHANG, SANDY S · 2014 to 2015
$398k
NCI NIH HHS P30 CA016359NCI NIH HHS R01 CA129037NCI NIH HHS R01 CA202816NCI NIH HHS R21 CA182280NCI NIH HHS R21CA182280NCI NIH HHS R21 CA200506NIA NIH HHS R21 AG043747
6 · The paper itself

Abstract

Repressor/activator protein 1 (RAP1) is a highly conserved telomere-interacting protein. Yeast Rap1 protects telomeres from non-homologous end joining (NHEJ), plays important roles in telomere length control and is involved in transcriptional gene regulation. However, a role for mammalian RAP1 in telomere end protection remains controversial. Here we present evidence that mammalian RAP1 is essential to protect telomere from homology directed repair (HDR) of telomeres. RAP1 cooperates with the basic domain of TRF2 (TRF2(B)) to repress PARP1 and SLX4 localization to telomeres. Without RAP1 and TRF2(B), PARP1 and SLX4 HR factors promote rapid telomere resection, resulting in catastrophic telomere loss and the generation of telomere-free chromosome fusions in both mouse and human cells. The RAP1 Myb domain is required to repress both telomere loss and formation of telomere-free fusions. Our results highlight the importance of the RAP1-TRF2 heterodimer in protecting telomeres from inappropriate processing by the HDR pathway.

Indexed as

Gene DeletionAnimalsCell LineDNA-Binding ProteinsDNA RepairFibroblastsGene Expression RegulationGenomic InstabilityHumansMiceProtein TransportRecombinant ProteinsShelterin ComplexTelomereTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2DNA-Binding ProteinsPARPBP protein, humanRecombinant ProteinsShelterin ComplexTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2TERF2IP protein, humanTERF2IP protein, mouseTERF2 protein, humanTRF2 protein, mouse

Identifiers

PMID26941064
PMCPMC4785230
OpenAlexW2334974904

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.