Evidence map›Paper›PMID 26055325›Full record

ArticleMolecular and cellular biology2015

Genetic Inactivation of ATRX Leads to a Decrease in the Amount of Telomeric Cohesin and Level of Telomere Transcription in Human Glioma Cells.

Rita Eid, Marie-Véronique Demattei, Harikleia Episkopou, Corinne Augé-Gouillou, Anabelle Decottignies, Nathalie Grandin, Michel Charbonneau

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. A Tale of Two States: Pluripotency Regulation of Telomeres.Frontiers in cell and developmental biology · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Functional Loss ofMolecular cancer research : MCR · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. New insights into cohesin loading.Current genetics · 2018
    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

7 authors at 4 institutions in 2 countries.

Rita EidUMR CNRS 7292, Université François-Rabelais de Tours, Tours, France.
Marie-Véronique DematteiUMR CNRS 7292, Université François-Rabelais de Tours, Tours, France.
Harikleia EpiskopouGenetic and Epigenetic Alterations of Genomes, de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Corinne Augé-GouillouEquipe Associée 6306, Instabilité Génétique et Cancer, Université François-Rabelais de Tours, Tours, France.
Anabelle DecottigniesGenetic and Epigenetic Alterations of Genomes, de Duve Institute, Catholic University of Louvain, Brussels, Belgium.
Nathalie GrandinUMR CNRS 7292, Université François-Rabelais de Tours, Tours, France.
Michel CharbonneauUMR CNRS 7292, Université François-Rabelais de Tours, Tours, France michel.charbonneau@univ-tours.fr.
Université de Tours · FRCentre National de la Recherche Scientifique · FRde Duve Institute · BEUCLouvain · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in ATRX (alpha thalassemia/mental retardation syndrome X-linked), a chromatin-remodeling protein, are associated with the telomerase-independent ALT (alternative lengthening of telomeres) pathway of telomere maintenance in several types of cancer, including human gliomas. In telomerase-positive glioma cells, we found by immunofluorescence that ATRX localized not far from the chromosome ends but not exactly at the telomere termini. Chromatin immunoprecipitation (ChIP) experiments confirmed a subtelomeric localization for ATRX, yet short hairpin RNA (shRNA)-mediated genetic inactivation of ATRX failed to trigger the ALT pathway. Cohesin has been recently shown to be part of telomeric chromatin. Here, using ChIP, we showed that genetic inactivation of ATRX provoked diminution in the amount of cohesin in subtelomeric regions of telomerase-positive glioma cells. Inactivation of ATRX also led to diminution in the amount of TERRAs, noncoding RNAs resulting from transcription of telomeric DNA, as well as to a decrease in RNA polymerase II (RNAP II) levels at the telomeres. Our data suggest that ATRX might establish functional interactions with cohesin on telomeric chromatin in order to control TERRA levels and that one or the other or both of these events might be relevant to the triggering of the ALT pathway in cancer cells that exhibit genetic inactivation of ATRX.

Indexed as

Transcription, GeneticCell Cycle ProteinsCell Line, TumorChromatinChromosomal Proteins, Non-HistoneCohesinsDNA HelicasesGliomaHumansNuclear ProteinsRNA InterferenceRNA Polymerase IIRNA, UntranslatedTelomeraseTelomereTelomere HomeostasisATRX protein, humanCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsDNA HelicasesNuclear ProteinsRNA Polymerase IIRNA, UntranslatedTelomeraseX-linked Nuclear Protein

Identifiers

PMID26055325
PMCPMC4508314
OpenAlexW1779155311

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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.