Evidence map›Paper›PMID 23302691›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

H1 linker histone promotes epigenetic silencing by regulating both DNA methylation and histone H3 methylation.

Seung-Min Yang, Byung Ju Kim, Laura Norwood Toro, Arthur I Skoultchi

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
7.0field-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

73 citing papers in PubMed, 123 citations in OpenAlex.

  1. The Spectrum and Clinical Impact of Epigenetic Modifier Mutations in Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
  8. Innate immune training in the neonatal response to sepsis.Molecular medicine (Cambridge, Mass.) · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Nucleosome destabilization by polyamines.Archives of biochemistry and biophysics · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

13 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

4 authors at 1 institution in 1 country.

Seung-Min YangDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Byung Ju Kim
Laura Norwood Toro
Arthur I Skoultchi
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
IN VIVO ANALYSIS OF MOUSE H1 HISTONE FUNCTIONR01CA079057 · NCI · YESHIVA UNIVERSITY · PI SKOULTCHI, ARTHUR I · 1998 to 2013
$5.4M
In Vivo Analysis of Mouse H1 Histone FunctionR56CA079057 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SKOULTCHI, ARTHUR I · 2008 to 2008
$250k
NCI NIH HHS 2P30CA13330NCI NIH HHS CA079057NCI NIH HHS P30 CA013330NCI NIH HHS R01 CA079057NCI NIH HHS R56 CA079057
6 · The paper itself

Abstract

Epigenetic silencing in mammals involves DNA methylation and posttranslational modifications of core histones. Here we show that the H1 linker histone plays a key role in regulating both DNA methylation and histone H3 methylation at the H19 and Gtl2 loci in mouse ES cells. Some, but not all, murine H1 subtypes interact with DNA methyltransferases DNMT1 and DNMT3B. The interactions are direct and require a portion of the H1 C-terminal domain. Expression of an H1 subtype that interacts with DNMT1 and DNMT3B in ES cells leads to their recruitment and DNA methylation of the H19 and Gtl2 imprinting control regions. H1 also interferes with binding of the SET7/9 histone methyltransferase to the imprinting control regions, inhibiting production of an activating methylation mark on histone H3 lysine 4. H1-dependent recruitment of DNMT1 and DNMT3B and interference with the binding of SET7/9 also were observed with chromatin reconstituted in vitro. The data support a model in which H1 plays an active role in helping direct two processes that lead to the formation of epigenetic silencing marks. The data also provide evidence for functional differences among the H1 subtypes expressed in somatic mammalian cells.

Indexed as

DNA MethylationEpigenesis, GeneticAnimalsBlotting, WesternCells, CulturedChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BEmbryonic Stem CellsGene ExpressionGenomic ImprintingHistone-Lysine N-MethyltransferaseHistonesMethylationMiceChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BDnmt1 protein, mouseH19 long non-coding RNAHistone-Lysine N-MethyltransferaseHistonesMEG3 non-coding RNA, mouseProtein IsoformsRNA, Long Noncoding

Identifiers

PMID23302691
PMCPMC3562819
OpenAlexW2011043347

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.