Evidence map›Paper›PMID 17306846›Full record

ReviewMutation research2007

Connections between epigenetic gene silencing and human disease.

Timothy J Moss, Lori L Wallrath

Open access · greenAbstract readReview
In one paragraph

Review in Mutation research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 126 citations in OpenAlex.

  1. Review
  2. Physical modeling of nucleosome clustering in euchromatin resulting from interactions between epigenetic reader proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Molecular mechanisms of alcohol's effects on the human body: A review and update.Journal of biochemical and molecular toxicology · 2023
    Review
  5. Review
  6. The Epigenetic Role of Vitamin C in Neurodevelopment.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Physical modeling of the heritability and maintenance of epigenetic modifications.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. The functional role of microRNAs in alcoholic liver injury.Journal of cellular and molecular medicine · 2014
    Review
  18. Review
  19. Article
  20. Epigenetics--new frontier for alcohol research.Alcohol research : current reviews · 2013
    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

2 authors at 1 institution in 1 country.

Timothy J MossDepartment of Biochemistry, 3136 MERF, University of Iowa, Iowa City, IA 52242, USA.
Lori L Wallrath
University of Iowa · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
Mechanisms of Gene SilencingR01GM061513 · NIGMS · UNIVERSITY OF IOWA · PI WALLRATH, LORI L · 2001 to 2009
$2.5M
NIGMS NIH HHS GM61513NIGMS NIH HHS R01 GM061513NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

Alterations in epigenetic gene regulation are associated with human disease. Here, we discuss connections between DNA methylation and histone methylation, providing examples in which defects in these processes are linked with disease. Mutations in genes encoding DNA methyltransferases and proteins that bind methylated cytosine residues cause changes in gene expression and alterations in the patterns of DNA methylation. These changes are associated with cancer and congenital diseases due to defects in imprinting. Gene expression is also controlled through histone methylation. Altered levels of methyltransferases that modify lysine 27 of histone H3 (K27H3) and lysine 9 of histone H3 (K9H3) correlate with changes in Rb signaling and disruption of the cell cycle in cancer cells. The K27H3 mark recruits a Polycomb complex involved in regulating stem cell pluripotency, silencing of developmentally regulated genes, and controlling cancer progression. The K9H3 methyl mark recruits HP1, a structural protein that plays a role in heterochromatin formation, gene silencing, and viral latency. Cells exhibiting altered levels of HP1 are predicted to show a loss of silencing at genes regulating cancer progression. Gene silencing through K27H3 and K9H3 can involve histone deacetylation and DNA methylation, suggesting cross talk between epigenetic silencing systems through direct interactions among the various players. The reversible nature of these epigenetic modifications offers therapeutic possibilities for a wide spectrum of disease.

Indexed as

Epigenesis, GeneticGene SilencingMutationAnimalsChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA (Cytosine-5-)-MethyltransferasesDNA MethylationHistonesHumansMethyltransferasesModels, BiologicalModels, GeneticRepressor ProteinsChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA (Cytosine-5-)-MethyltransferasesHistonesMethyltransferasesRepressor ProteinsSUV39H1 protein, human

Identifiers

PMID17306846
PMCPMC1892579
OpenAlexW2077810304

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.