Evidence map›Paper›PMID 19427507›Full record

ArticleMutation research2009

Epigenetic control of mammalian LINE-1 retrotransposon by retinoblastoma proteins.

Diego E Montoya-Durango, Yongqing Liu, Ivo Teneng, Ted Kalbfleisch, Mary E Lacy, Marlene C Steffen, Kenneth S Ramos

Open access · greenAbstract read
In one paragraph

Article in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
12.2field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 99 citations in OpenAlex.

  1. LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. The reconstruction of evolutionary dynamics of processed pseudogenes indicates deep silencing of "retrobiome" in naked mole rat.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Is There a Histone Code for Cellular Quiescence?Frontiers in cell and developmental biology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Precision prevention: A focused response to shifting paradigms in healthcare.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review

3 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

7 authors at 2 institutions in 1 country.

Diego E Montoya-DurangoDepartment of Biochemistry and Molecular Biology and Center for Genetics and Molecular Medicine, University of Louisville School of Medicine Health Sciences Center, Louisville, KY 40202, USA.
Yongqing Liu
Ivo Teneng
Ted Kalbfleisch
Mary E Lacy
Marlene C Steffen
Kenneth S Ramos
University of Louisville · USUniversity of Louisville Hospital · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI RAMOS, KENNETH S. · 2007 to 2010
$4.4M
MOLECULAR MECHANISMS OF VASCULAR TOXICITYR01ES004849 · NIEHS · UNIVERSITY OF LOUISVILLE · PI RAMOS, KENNETH S · 1988 to 2005
$1.3M
NIEHS NIH HHS ES014443NIEHS NIH HHS ES04849NIEHS NIH HHS P30 ES014443NIEHS NIH HHS R01 ES004849
6 · The paper itself

Abstract

Long interspersed nuclear elements (LINEs or L1 elements) are targeted for epigenetic silencing during early embryonic development and remain inactive in most cells and tissues. Here we show that E2F-Rb family complexes participate in L1 elements epigenetic regulation via nucleosomal histone modifications and recruitment of histone deacetylases (HDACs) HDAC1 and HDAC2. Our experiments demonstrated that (i) Rb and E2F interact with human and mouse L1 elements, (ii) L1 elements are deficient in both heterochromatin-associated histone marks H3 tri methyl K9 and H4 tri methyl K20 in Rb family triple knock out (Rb, p107, and p130) fibroblasts (TKO), (iii) L1 promoter exhibits increased histone H3 acetylation in the absence of HDAC1 and HDAC2 recruitment, (iv) L1 expression in TKO fibroblasts is upregulated compared to wild type counterparts, (v) L1 expression increases in the presence of the HDAC inhibitor TSA. On the basis of these findings we propose a model in which L1 sequences throughout the genome serve as centers for heterochromatin formation in an Rb family-dependent manner. As such, Rb proteins and L1 elements may play key roles in heterochromatin formation beyond pericentromeric chromosomal regions. These findings describe a novel mechanism of L1 reactivation in mammalian cells mediated by failure of corepressor protein recruitment by Rb, loss of histone epigenetic marks, heterochromatin formation, and increased histone H3 acetylation.

Indexed as

Epigenesis, GeneticLong Interspersed Nucleotide ElementsAcetylationAnimalsCell LineCells, CulturedDNAE2F Transcription FactorsHeLa CellsHeterochromatinHistone DeacetylasesHistonesHumansMiceMice, KnockoutMultiprotein ComplexesDNAE2F Transcription FactorsHeterochromatinHistone DeacetylasesHistonesMultiprotein ComplexesRbl1 protein, mouseRbl2 protein, mouseRetinoblastoma-Like Protein p107Retinoblastoma-Like Protein p130Retinoblastoma Protein

Identifiers

PMID19427507
PMCPMC3418809
OpenAlexW1988000848

What OpenQuestion holds

Textmetadata
LicenceTDM
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.