Evidence map›Paper›PMID 21317192›Full record

ArticleNucleic acids research2011

Integrated genome-wide chromatin occupancy and expression analyses identify key myeloid pro-differentiation transcription factors repressed by Myb.

Liang Zhao, Evgeny A Glazov, Diwakar R Pattabiraman, Faisal Al-Owaidi, Ping Zhang, Matthew A Brown, Paul J Leo, Thomas J Gonda

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
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  7. Review
  8. Article
  9. Article
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  12. Review
  13. Synthetic oleanane triterpenoids suppressFrontiers in oncology · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

7 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

8 authors at 1 institution in 1 country.

Liang ZhaoThe University of Queensland Diamantina Institute, Brisbane, Queensland 4102, Australia.
Evgeny A Glazov
Diwakar R Pattabiraman
Faisal Al-Owaidi
Ping Zhang
Matthew A Brown
Paul J Leo
Thomas J Gonda
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To gain insight into the mechanisms by which the Myb transcription factor controls normal hematopoiesis and particularly, how it contributes to leukemogenesis, we mapped the genome-wide occupancy of Myb by chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-Seq) in ERMYB myeloid progenitor cells. By integrating the genome occupancy data with whole genome expression profiling data, we identified a Myb-regulated transcriptional program. Gene signatures for leukemia stem cells, normal hematopoietic stem/progenitor cells and myeloid development were overrepresented in 2368 Myb regulated genes. Of these, Myb bound directly near or within 793 genes. Myb directly activates some genes known critical in maintaining hematopoietic stem cells, such as Gfi1 and Cited2. Importantly, we also show that, despite being usually considered as a transactivator, Myb also functions to repress approximately half of its direct targets, including several key regulators of myeloid differentiation, such as Sfpi1 (also known as Pu.1), Runx1, Junb and Cebpb. Furthermore, our results demonstrate that interaction with p300, an established coactivator for Myb, is unexpectedly required for Myb-mediated transcriptional repression. We propose that the repression of the above mentioned key pro-differentiation factors may contribute essentially to Myb's ability to suppress differentiation and promote self-renewal, thus maintaining progenitor cells in an undifferentiated state and promoting leukemic transformation.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsBinding SitesCells, CulturedChromatinChromatin ImmunoprecipitationGene Expression ProfilingGene Regulatory NetworksGenomicsHistonesLeukemiaMiceMice, Inbred C57BLMyeloid Progenitor CellsMyelopoiesisChromatinHistonesp300-CBP-Associated Factorp300-CBP Transcription FactorsProto-Oncogene Proteins c-mybRepressor ProteinsTranscription Factors

Identifiers

PMID21317192
PMCPMC3113568
OpenAlexW2170251269

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.