Evidence map›Paper›PMID 7848278›Full record

ArticleThe Biochemical journal1995

The effect of histone H1 and DNA methylation on transcription.

C A Johnson, J P Goddard, R L Adams

Abstract read
In one paragraph

Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Methylation of the minimal promoter of an embryonic globin gene silences transcription in primary erythroid cells.Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  8. Article
  9. Article
  10. Article
  11. 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

3 authors.

C A JohnsonInstitute of Biomedical and Life Sciences, University of Glasgow, UK.
J P Goddard
R L Adams

Funding

Wellcome Trust
6 · The paper itself

Abstract

We have previously shown that DNA methylation acts as a focus for the formation of inactive chromatin in vivo. We have investigated the mechanism further by in vitro transcription of a template containing two tRNA genes and an extensive (G+C)-rich sequence characteristic of a CpG island. The extent of transcription from the unmethylated or fully methylated template was assayed in the presence of varied levels of histone H1. The transcriptional activity of both templates was inhibited by increasing amounts of histone H1, although inhibition with the methylated template occurs at a lower H1:DNA ratio. The H1c variant shows the greatest preferential inhibition of the methylated template. We demonstrated that histone H1 complexed to DNA is one of the factors that inhibits transcription by preventing the formation of initiation complexes, particularly on methylated template, rather than the formation of disordered H1.DNA aggregates.

Indexed as

Ammonium SulfateCell FractionationCell NucleusDNAEscherichia coliHistonesHumansMethylationPlasmidsRNA, Transfer, ArgRNA, Transfer, LeuTemplates, GeneticTranscription, GeneticAmmonium SulfateDNAHistonesRNA, Transfer, ArgRNA, Transfer, Leu

Identifiers

PMID7848278
PMCPMC1136328

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.