Evidence map›Paper›PMID 22577155›Full record

SynthesisOncotarget2012

On the presence and role of human gene-body DNA methylation.

Daudi Jjingo, Andrew B Conley, Soojin V Yi, Victoria V Lunyak, I King Jordan

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 303 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
303citing papers in PubMed, 1 pooled it
15.2field-weighted citation impact, top 1% 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

303 citing papers in PubMed, 1 synthesis or guideline pooled it, 542 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Epigenomic methylome landscape of promoters in vertebrate genomes.bioRxiv : the preprint server for biology · 2026
    Article
  11. Promoter Methylation-Expression Coupling of Gliogenesis Genes inInternational journal of molecular sciences · 2026
    Article
  12. Epigenetics and chromatin structure regulatebioRxiv : the preprint server for biology · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

243 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

5 authors at 3 institutions in 2 countries.

Daudi JjingoSchool of Biology, Georgia Institute of Technology, Atlanta, GA 30332, USA.
Andrew B Conley
Soojin V Yi
Victoria V Lunyak
I King Jordan
Georgia Institute of Technology · USBuck Institute for Research on Aging · USPanAmerican Bioinformatics Institute · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation of promoter sequences is a repressive epigenetic mark that down-regulates gene expression. However, DNA methylation is more prevalent within gene-bodies than seen for promoters, and gene-body methylation has been observed to be positively correlated with gene expression levels. This paradox remains unexplained, and accordingly the role of DNA methylation in gene-bodies is poorly understood. We addressed the presence and role of human gene-body DNA methylation using a meta-analysis of human genome-wide methylation, expression and chromatin data sets. Methylation is associated with transcribed regions as genic sequences have higher levels of methylation than intergenic or promoter sequences. We also find that the relationship between gene-body DNA methylation and expression levels is non-monotonic and bell-shaped. Mid-level expressed genes have the highest levels of gene-body methylation, whereas the most lowly and highly expressed sets of genes both have low levels of methylation. While gene-body methylation can be seen to efficiently repress the initiation of intragenic transcription, the vast majority of methylated sites within genes are not associated with intragenic promoters. In fact, highly expressed genes initiate the most intragenic transcription inconsistent with the previously held notion that gene-body methylation serves to repress spurious intragenic transcription to allow for efficient transcriptional elongation. These observations lead us to propose a model to explain the presence of human gene-body methylation. This model holds that the repression of intragenic transcription by gene-body methylation is largely epiphenomenal, and suggests that gene-body methylation levels are predominantly shaped via the accessibility of the DNA to methylating enzyme complexes.

Indexed as

DNA MethylationPromoter Regions, GeneticChromatinDatabases, GeneticDNAGenome, HumanHumansTranscription, GeneticChromatinDNA

Identifiers

PMID22577155
PMCPMC3380580
OpenAlexW2162178715

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.