Evidence map›Paper›PMID 26208222›Full record

ArticlePloS one2015

c-Myb Binding Sites in Haematopoietic Chromatin Landscapes.

Mads Bengtsen, Kjetil Klepper, Sveinung Gundersen, Ignacio Cuervo, Finn Drabløs, Eivind Hovig, Geir Kjetil Sandve, Odd Stokke Gabrielsen, Ragnhild Eskeland

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
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  12. Review
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  14. Article
  15. Dual Mechanism ofMolecular and cellular biology · 2017
    Article
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  17. 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

9 authors at 3 institutions in 1 country.

Mads BengtsenDepartment of Biosciences, University of Oslo, Oslo, Norway.
Kjetil KlepperDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Sveinung GundersenDepartment of Informatics, University of Oslo, Oslo, Norway.
Ignacio CuervoDepartment of Biosciences, University of Oslo, Oslo, Norway.
Finn DrabløsDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Eivind HovigDepartment of Informatics, University of Oslo, Oslo, Norway; Department of Tumour Biology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway; Department of Medical Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Geir Kjetil SandveDepartment of Informatics, University of Oslo, Oslo, Norway.
Odd Stokke GabrielsenDepartment of Biosciences, University of Oslo, Oslo, Norway.
Ragnhild EskelandDepartment of Biosciences, University of Oslo, Oslo, Norway.
University of Oslo · NONorwegian University of Science and Technology · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Strict control of tissue-specific gene expression plays a pivotal role during lineage commitment. The transcription factor c-Myb has an essential role in adult haematopoiesis and functions as an oncogene when rearranged in human cancers. Here we have exploited digital genomic footprinting analysis to obtain a global picture of c-Myb occupancy in the genome of six different haematopoietic cell-types. We have biologically validated several c-Myb footprints using c-Myb knockdown data, reporter assays and DamID analysis. We show that our predicted conserved c-Myb footprints are highly dependent on the haematopoietic cell type, but that there is a group of gene targets common to all cell-types analysed. Furthermore, we find that c-Myb footprints co-localise with active histone mark H3K4me3 and are significantly enriched at exons. We analysed co-localisation of c-Myb footprints with 104 chromatin regulatory factors in K562 cells, and identified nine proteins that are enriched together with c-Myb footprints on genes positively regulated by c-Myb and one protein enriched on negatively regulated genes. Our data suggest that c-Myb is a transcription factor with multifaceted target regulation depending on cell type.

Indexed as

Binding SitesCell DifferentiationChromatinDNA FootprintingGene Expression RegulationGenome-Wide Association StudyHematopoiesisHistonesHumansK562 CellsProtein BindingProto-Oncogene Proteins c-mybTranscription FactorsTranscription, GeneticChromatinHistonesProto-Oncogene Proteins c-mybTranscription Factors

Identifiers

PMID26208222
PMCPMC4514710
OpenAlexW1928277753

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.