Evidence map›Paper›PMID 21862875›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Inhibition of activated pericentromeric SINE/Alu repeat transcription in senescent human adult stem cells reinstates self-renewal.

Jianrong Wang, Glenn J Geesman, Sirkka Liisa Hostikka, Michelle Atallah, Benjamin Blackwell, Elbert Lee, Peter J Cook, Bogdan Pasaniuc, Goli Shariat, Eran Halperin and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A multi-omics analysis of human fibroblasts overexpressing anbioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
  7. LINE-1 retrotransposon activation drives age-associated inflammationContemporary oncology (Poznan, Poland) · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Transposon control as a checkpoint for tissue regeneration.Development (Cambridge, England) · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 2 countries.

Jianrong WangSchool of Biology, Georgia Institute of Technology, Atlanta, GA, USA.
Glenn J Geesman
Sirkka Liisa Hostikka
Michelle Atallah
Benjamin Blackwell
Elbert Lee
Peter J Cook
Bogdan Pasaniuc
Goli Shariat
Eran Halperin
Marek Dobke
Michael G Rosenfeld
I King Jordan
Victoria V Lunyak
Buck Institute for Research on Aging · USGeorgia Institute of Technology · USHoward Hughes Medical Institute · USTel Aviv University · ILUniversity of California, Berkeley · USUniversity of California, San Diego · US

Funding

REGULATION OF NEUROENDOCRINE SWITCHING EVENTSR37DK039949 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1987 to 2020
$12.3M
Ligand Regulated Epigenetic/Nuclear Architectural Strategies and Human DiseaseR01NS034934 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1995 to 2013
$6.8M
Interdisciplinary Research Consortium in GeroscienceUL1DE019608 · NIDCR · BUCK INSTITUTE FOR RESEARCH ON AGING · PI LITHGOW, GORDON J · 2008 to 2011
$4.0M
Howard Hughes Medical InstituteNIDCR NIH HHS UL1 DE019608NIDDK NIH HHS R37 DK039949NINDS NIH HHS R01 NS034934
6 · The paper itself

Abstract

Cellular aging is linked to deficiencies in efficient repair of DNA double strand breaks and authentic genome maintenance at the chromatin level. Aging poses a significant threat to adult stem cell function by triggering persistent DNA damage and ultimately cellular senescence. Senescence is often considered to be an irreversible process. Moreover, critical genomic regions engaged in persistent DNA damage accumulation are unknown. Here we report that 65% of naturally occurring repairable DNA damage in self-renewing adult stem cells occurs within transposable elements. Upregulation of Alu retrotransposon transcription upon ex vivo aging causes nuclear cytotoxicity associated with the formation of persistent DNA damage foci and loss of efficient DNA repair in pericentric chromatin. This occurs due to a failure to recruit of condensin I and cohesin complexes. Our results demonstrate that the cytotoxicity of induced Alu repeats is functionally relevant for the human adult stem cell aging. Stable suppression of Alu transcription can reverse the senescent phenotype, reinstating the cells' self-renewing properties and increasing their plasticity by altering so-called "master" pluripotency regulators.

Indexed as

Alu ElementsCellular SenescenceDNA DamageTranscriptional ActivationAdenosine TriphosphatasesAdipose TissueAdult Stem CellsCell Cycle ProteinsCell NucleusCell ProliferationCentromereChromatinChromosomal Proteins, Non-HistoneChromosomes, HumanCohesinsDNA-Binding ProteinsAdenosine TriphosphatasesCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinscondensin complexesDNA-Binding ProteinsH2AX protein, humanHistonesMultiprotein Complexes

Identifiers

PMID21862875
PMCPMC3218602
OpenAlexW1974423729

What OpenQuestion holds

Textmetadata
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.