Evidence map›Paper›PMID 21760879›Full record

ArticlePloS one2011

A siRNA-based screen for genes involved in chromosome end protection.

Daniel H Lackner, Daniel Durocher, Jan Karlseder

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Roles of RNA-Binding Proteins in DNA Damage Response.International journal of molecular sciences · 2016
    Review
  6. Article
  7. Article
  8. Article
  9. RNA splicing: a new player in the DNA damage response.International journal of cell biology · 2013
    Review
  10. Article
  11. 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 2 institutions in 2 countries.

Daniel H LacknerMolecular and Cellular Biology Department, The Salk Institute for Biological Studies, La Jolla, California, United States of America.
Daniel Durocher
Jan Karlseder
Salk Institute for Biological Studies · USMount Sinai Hospital · CA

Funding

Understanding ALT activation in C. elegans and human cellsR01GM087476 · NIGMS · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN · 2009 to 2017
$3.2M
Telomeric Function in Aging SyndromesR01AG025837 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI KARLSEDER, JAN · 2006 to 2010
$1.5M
NIA NIH HHS R01 AG025837NIGMS NIH HHS R01 GM087476
6 · The paper itself

Abstract

Telomeres are nucleoprotein complexes which protect the ends of linear chromosomes from detection as DNA damage and provide a sequence buffer against replication-associated shortening. In mammals, telomeres consist of repetitive DNA sequence (TTAGGG) and associated proteins. The telomeric core complex is called shelterin and is comprised of the proteins TRF1, TRF2, POT1, TIN2, TPP1 and RAP1. Excessive telomere shortening or de-protection of telomeres through the loss of shelterin subunits allows the detection of telomeres as DNA damage, which can be visualized as DNA damage protein foci at chromosome ends called TIF (Telomere Dysfunction-Induced Foci). We sought to exploit the TIF phenotype as marker for telomere dysfunction to identify novel genes involved in telomere protection by siRNA-mediated knock-down of a set of 386 candidates. Here we report the establishment, specificity and feasibility of such a screen and the results of the genes tested. Only one of the candidate genes showed a unique TIF phenotype comparable to the suppression of the main shelterin components TRF2 or TRF1 and that gene was identified as a TRF1-like pseudogene. We also identified a weak TIF phenotype for SKIIP (SNW1), a splicing factor and transcriptional co-activator. However, the knock-down of SKIIP also induced a general, not telomere-specific DNA damage response, which complicates conclusions about a telomeric role. In summary, this report is a technical demonstration of the feasibility of a cell-based screen for telomere deprotection with the potential of scaling it to a high-throughput approach.

Indexed as

DNA DamageGene Knockdown TechniquesHeLa CellsHumansPhenotypeRNA, Small InterferingShelterin ComplexTelomereTelomere-Binding ProteinsACD protein, humanRNA, Small InterferingShelterin ComplexTelomere-Binding Proteins

Identifiers

PMID21760879
PMCPMC3121770
OpenAlexW2031358152

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.