Evidence map›Paper›PMID 25961132›Full record

ArticleNucleus (Austin, Tex.)2015

A beginning of the end: new insights into the functional organization of telomeres.

Ashley M Wood, Kyle Laster, Ellen L Rice, Steven T Kosak

Open access · goldAbstract read
In one paragraph

Article in Nucleus (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The Intra- and Extra-Telomeric Role of TRF2 in the DNA Damage Response.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. The Role of Ku70 as a Cytosolic DNA Sensor in Innate Immunity and Beyond.Frontiers in cellular and infection microbiology · 2021
    Review
  17. Review
  18. Review
  19. Mitochondria, Telomeres and Telomerase Subunits.Frontiers in cell and developmental biology · 2019
    Review
  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

4 authors at 1 institution in 1 country.

Ashley M Wooda Department of Cell and Molecular Biology; Feinberg School of Medicine; Northwestern University ; Chicago , IL , USA.
Kyle Laster
Ellen L Rice
Steven T Kosak
Northwestern University · US

Funding

Mentoring For Success: Developing Fundamental Skills For Biomedical ResearchR25GM079300 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MCGEE, RICHARD · 2007 to 2020
$6.6M
Self-Organization of the Human GenomeDP2OD008717 · OD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KOSAK, STEVEN TODD · 2011 to 2016
$2.8M
NIGMS NIH HHS R25 GM079300NIH HHS DP2 OD008717NIH HHS DP2 OD008717-0
6 · The paper itself

Abstract

Ever since the first demonstration of their repetitive sequence and unique replication pathway, telomeres have beguiled researchers with how they function in protecting chromosome ends. Of course much has been learned over the years, and we now appreciate that telomeres are comprised of the multimeric protein/DNA shelterin complex and that the formation of t-loops provides protection from DNA damage machinery. Deriving their name from D-loops, t-loops are generated by the insertion of the 3' overhang into telomeric repeats facilitated by the binding of TRF2. Recent studies have uncovered novel forms of chromosome end-structure that may implicate telomere organization in cellular processes beyond its essential role in telomere protection and homeostasis. In particular, we have recently described that t-loops form in a TRF2-dependent manner at interstitial telomere repeat sequences, which we termed interstitial telomere loops (ITLs). These structures are also dependent on association of lamin A/C, a canonical component of the nucleoskeleton that is mutated in myriad human diseases, including human segmental progeroid syndromes. Since ITLs are associated with telomere stability and require functional lamin A/C, our study suggests a mechanistic link between cellular aging (replicative senescence induced by telomere shortening) and organismal aging (modeled by Hutchinson Gilford Progeria Syndrome). Here we speculate on other potential ramifications of ITL formation, from gene expression to genome stability to chromosome structure.

Indexed as

Telomere ShorteningCell DivisionDNAGene Expression RegulationGenomic InstabilityHeterochromatinHumansLamin Type ANucleic Acid ConformationProgeriaShelterin ComplexSignal TransductionTelomeraseTelomereTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2DNAHeterochromatinLamin Type ALMNA protein, humanShelterin ComplexTelomeraseTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2TERF2 protein, humanTERT protein, humanagingchromosome loopingchromosome structuregenome stabilitynuclear laminatelomere

Identifiers

PMID25961132
PMCPMC4615733
OpenAlexW1488008687

What OpenQuestion holds

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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.