Evidence map›Paper›PMID 16222338›Full record

ArticleThe EMBO journal2005

PU.1 inhibits the erythroid program by binding to GATA-1 on DNA and creating a repressive chromatin structure.

Tomas Stopka, Derek F Amanatullah, Michael Papetti, Arthur I Skoultchi

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 150 citations in OpenAlex.

  1. Article
  2. Article
  3. iScience · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Stochastic multistationarity in a model of the hematopoietic stem cell differentiation network.Proceedings of the ... IEEE Conference on Decision & Control. IEEE Conference on Decision & Control · 2018
    Article
  15. Article
  16. The zebrafish: A fintastic model for hematopoietic development and disease.Wiley interdisciplinary reviews. Developmental biology · 2018
    Review
  17. Review
  18. Article
  19. Review
  20. Article

23 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.

Tomas StopkaDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
Derek F Amanatullah
Michael Papetti
Arthur I Skoultchi
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Control of Erythroid Cell Division and DifferentiationR01HL078381 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI SKOULTCHI, ARTHUR I · 2004 to 2008
$2.1M
Role of GATA-1 in p21 Gene TranscriptionF32HL077242 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI PAPETTI, MICHAEL J · 2004 to 2006
$149k
NCI NIH HHS 2P30CA13330NCI NIH HHS P30 CA013330NHLBI NIH HHS 1F32 HL077242-0102NHLBI NIH HHS HL78381NHLBI NIH HHS R01 HL078381NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32 GM07288
6 · The paper itself

Abstract

Transcriptional repression mechanisms are important during differentiation of multipotential hematopoietic progenitors, where they are thought to regulate lineage commitment and to extinguish alternative differentiation programs. PU.1 and GATA-1 are two critical hematopoietic transcription factors that physically interact and mutually antagonize each other's transcriptional activity and ability to promote myeloid and erythroid differentiation, respectively. We find that PU.1 inhibits the erythroid program by binding to GATA-1 on its target genes and organizing a complex of proteins that creates a repressive chromatin structure containing lysine-9 methylated H3 histones and heterochromatin protein 1. Although these features are thought to be stable aspects of repressed chromatin, we find that silencing of PU.1 expression leads to removal of the repression complex, loss of the repressive chromatin marks and reactivation of the erythroid program. This process involves incorporation of the replacement histone variant H3.3 into nucleosomes. Repression of one transcription factor bound to DNA by another transcription factor not on the DNA represents a new mechanism for downregulating an alternative gene expression program during lineage commitment of multipotential hematopoietic progenitors.

Indexed as

ErythropoiesisGene Expression RegulationAnimalsCell LineChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNADNA-Binding ProteinsGATA Transcription FactorsGene SilencingHistidineHistonesMethylationMiceProtein BindingChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNADNA-Binding ProteinsGATA Transcription FactorsHistidineHistonesProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID16222338
PMCPMC1276718
OpenAlexW2121864465

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.