Evidence map›Paper›PMID 26942192›Full record

ArticleBioMed research international2016

E2A Antagonizes PU.1 Activity through Inhibition of DNA Binding.

Jason H Rogers, Kristin S Owens, Jeffrey Kurkewich, Nathan Klopfenstein, Sangeeta R Iyer, M Celeste Simon, Richard Dahl

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

Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
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  5. 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

7 authors at 5 institutions in 1 country.

Jason H RogersCancer Research and Treatment Center, University of New Mexico, Albuquerque, NM 87131, USA.
Kristin S OwensCancer Research and Treatment Center, University of New Mexico, Albuquerque, NM 87131, USA.
Jeffrey KurkewichBiological Science, University of Notre Dame, Notre Dame, IN 46556, USA.
Nathan KlopfensteinDepartment of Microbiology and Immunology, Indiana University School of Medicine, South Bend, IN 46617, USA.
Sangeeta R IyerAbramson Family Cancer Research Institute, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
M Celeste SimonAbramson Family Cancer Research Institute, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104, USA.
Richard DahlCancer Research and Treatment Center, University of New Mexico, Albuquerque, NM 87131, USA; Biological Science, University of Notre Dame, Notre Dame, IN 46556, USA; Department of Microbiology and Immunology, Indiana University School of Medicine, South Bend, IN 46617, USA.
Cancer Research Institute · USIndiana University School of MedicineNew Mexico Cancer Center · USUniversity of New Mexico · USUniversity of Notre Dame · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antagonistic interactions between transcription factors contribute to cell fate decisions made by multipotent hematopoietic progenitor cells. Concentration of the transcription factor PU.1 affects myeloid/lymphoid development with high levels of PU.1 directing myeloid cell fate acquisition at the expense of B cell differentiation. High levels of PU.1 may be required for myelopoiesis in order to overcome inhibition of its activity by transcription factors that promote B cell development. The B cell transcription factors, E2A and EBF, are necessary for commitment of multipotential progenitors and lymphoid primed multipotential progenitors to lymphocytes. In this report we hypothesized that factors required for early B cell commitment would bind to PU.1 and antagonize its ability to induce myeloid differentiation. We investigated whether E2A and/or EBF associate with PU.1. We observed that the E2A component, E47, but not EBF, directly binds to PU.1. Additionally E47 represses PU.1-dependent transactivation of the MCSFR promoter through antagonizing PU.1's ability to bind to DNA. Exogenous E47 expression in hematopoietic cells inhibits myeloid differentiation. Our data suggest that E2A antagonism of PU.1 activity contributes to its ability to commit multipotential hematopoietic progenitors to the lymphoid lineages.

Indexed as

Basic Helix-Loop-Helix ProteinsB-LymphocytesCell DifferentiationCell LineCell LineageDNA-Binding ProteinsGene Expression Regulation, DevelopmentalHematopoietic Stem CellsMacrophage Colony-Stimulating FactorMyeloid CellsProtein BindingProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTranscription Factor 3Basic Helix-Loop-Helix ProteinsDNA-Binding ProteinsEBF1 protein, humanMacrophage Colony-Stimulating FactorProto-Oncogene ProteinsProto-Oncogene Protein Spi-1TCF3 protein, humanTrans-ActivatorsTranscription Factor 3

Identifiers

PMID26942192
PMCPMC4749766
OpenAlexW2292888378

What OpenQuestion holds

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LicenceCC BY
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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.