Evidence map›Paper›PMID 12556492›Full record

ArticleMolecular and cellular biology2003

Formation of a tissue-specific histone acetylation pattern by the hematopoietic transcription factor GATA-1.

Danielle L Letting, Carrie Rakowski, Mitchell J Weiss, Gerd A Blobel

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.8field-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

75 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
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  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Epigenetic and genetic mechanisms in red cell biology.Current opinion in hematology · 2014
    Review
  15. Article
  16. Article
  17. Transcriptional mechanisms underlying hemoglobin synthesis.Cold Spring Harbor perspectives in medicine · 2013
    Review
  18. Article
  19. Article
  20. Article

15 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 2 institutions in 1 country.

Danielle L LettingDivision of Hematology, Children's Hospital of Philadelphia and University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Carrie Rakowski
Mitchell J Weiss
Gerd A Blobel
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Transcriptional Networks Controlling Erythroid DifferentiationR01DK054937 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI Gerd A Blobel · 1999 to 2026
$12.8M
PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008216 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI EPSTEIN, DOUGLAS J · 1987 to 2023
$8.3M
NIDDK NIH HHS DK54937NIDDK NIH HHS R01 DK054937NIGMS NIH HHS T32 GM008216NIGMS NIH HHS T32GM008216
6 · The paper itself

Abstract

One function of lineage-restricted transcription factors may be to control the formation of tissue-specific chromatin domains. In erythroid cells, the beta-globin gene cluster undergoes developmentally regulated hyperacetylation of histones at the active globin genes and the locus control region (LCR). However, it is unknown which transcription factor(s) governs the establishment of this erythroid-specific chromatin domain. We measured histone acetylation at the beta-globin locus in the erythroid cell line G1E, which is deficient for the essential hematopoietic transcription factor GATA-1. Restoration of GATA-1 activity in G1E cells led to a substantial increase in acetylation of histones H3 and H4 at the beta-globin promoter and the LCR. Time course experiments showed that histone acetylation occurred rapidly after GATA-1 activation and coincided with globin gene expression, indicating that the effects of GATA-1 are direct. Moreover, increases in histone acetylation correlated with occupancy of GATA-1 and the acetyltransferase CBP at the locus in vivo. Together, these results suggest that GATA-1 and its cofactor CBP are essential for the formation of an erythroid-specific acetylation pattern that is permissive for high levels of gene expression.

Indexed as

AcetylationAcetyltransferasesAnimalsBinding SitesCell Cycle ProteinsCells, CulturedDNA-Binding ProteinsErythrocytesErythroid-Specific DNA-Binding FactorsGATA1 Transcription FactorGene Expression RegulationGlobinsHistone AcetyltransferasesHistonesLocus Control RegionMiceAcetyltransferasesCell Cycle ProteinsDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsGata1 protein, mouseGATA1 Transcription FactorGlobinsHistone AcetyltransferasesHistonesp300-CBP-Associated Factorp300-CBP Transcription FactorsReceptors, EstrogenRecombinant ProteinsTranscription Factors

Identifiers

PMID12556492
PMCPMC141148
OpenAlexW2004292212

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.