Evidence map›Paper›PMID 25911237›Full record

ArticleBlood2015

RUNX1 represses the erythroid gene expression program during megakaryocytic differentiation.

Olga N Kuvardina, Julia Herglotz, Stephan Kolodziej, Nicole Kohrs, Stefanie Herkt, Bartosch Wojcik, Thomas Oellerich, Jasmin Corso, Kira Behrens, Ashok Kumar and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
6.4field-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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Review
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  16. Role of MiRNA in the Regulation of Blood Group Expression.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Transcription Factor TAL1 in Erythropoiesis.Advances in experimental medicine and biology · 2024
    Review

20 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

18 authors at 6 institutions in 1 country.

Olga N KuvardinaGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Julia HerglotzHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany;
Stephan KolodziejGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Nicole KohrsGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Stefanie HerktGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Bartosch WojcikDepartment of Medicine, Hematology/Oncology, Johann-Wolfgang-Goethe University, Frankfurt am Main, Germany;
Thomas OellerichDepartment of Medicine, Hematology/Oncology, Johann-Wolfgang-Goethe University, Frankfurt am Main, Germany; German Cancer Consortium, Heidelberg, Germany; German Cancer Research Center, Heidelberg, Germany;
Jasmin CorsoBioanalytical Mass Spectrometry Group, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany;
Kira BehrensHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany;
Ashok KumarGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Helge HussongGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Henning UrlaubBioanalytical Mass Spectrometry Group, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany;
Joachim KochGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Hubert ServeDepartment of Medicine, Hematology/Oncology, Johann-Wolfgang-Goethe University, Frankfurt am Main, Germany; German Cancer Consortium, Heidelberg, Germany; German Cancer Research Center, Heidelberg, Germany;
Halvard BonigGerman Red Cross Blood Service and Institute for Transfusion Medicine and Immunohematology, Johann-Wolfgang-Goethe University, Frankfurt am Main, Germany; and.
Carol StockingHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany;
Michael A RiegerDepartment of Medicine, Hematology/Oncology, Johann-Wolfgang-Goethe University, Frankfurt am Main, Germany; German Cancer Consortium, Heidelberg, Germany; German Cancer Research Center, Heidelberg, Germany; LOEWE Center for Cell and Gene Therapy, Frankfurt, Germany.
Jörn LausenGeorg-Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany;
Georg Speyer Haus · DEGoethe University Frankfurt · DELeibniz Institute of Virology (LIV) · DEMax Planck Institute for Biophysical Chemistry · DEDeutschen Konsortium für Translationale Krebsforschung · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activity of antagonizing transcription factors represents a mechanistic paradigm of bidirectional lineage-fate control during hematopoiesis. At the megakaryocytic/erythroid bifurcation, the cross-antagonism of krueppel-like factor 1 (KLF1) and friend leukemia integration 1 (FLI1) has such a decisive role. However, how this antagonism is resolved during lineage specification is poorly understood. We found that runt-related transcription factor 1 (RUNX1) inhibits erythroid differentiation of murine megakaryocytic/erythroid progenitors and primary human CD34(+) progenitor cells. We show that RUNX1 represses the erythroid gene expression program during megakaryocytic differentiation by epigenetic repression of the erythroid master regulator KLF1. RUNX1 binding to the KLF1 locus is increased during megakaryocytic differentiation and counterbalances the activating role of T-cell acute lymphocytic leukemia 1 (TAL1). We found that corepressor recruitment by RUNX1 contributes to a block of the KLF1-dependent erythroid gene expression program. Our data indicate that the repressive function of RUNX1 influences the balance between erythroid and megakaryocytic differentiation by shifting the balance between KLF1 and FLI1 in the direction of FLI1. Taken together, we show that RUNX1 is a key player within a network of transcription factors that represses the erythroid gene expression program.

Indexed as

Antigens, CD34Basic Helix-Loop-Helix ProteinsCell DifferentiationCore Binding Factor Alpha 2 SubunitErythroid Precursor CellsErythropoiesisGene Expression RegulationHumansK562 CellsKruppel-Like Transcription FactorsMegakaryocyte Progenitor CellsMegakaryocytesProto-Oncogene ProteinsT-Cell Acute Lymphocytic Leukemia Protein 1ThrombopoiesisAntigens, CD34Basic Helix-Loop-Helix ProteinsCore Binding Factor Alpha 2 Subuniterythroid Kruppel-like factorKruppel-Like Transcription FactorsProto-Oncogene ProteinsRUNX1 protein, humanTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1

Identifiers

PMID25911237
PMCPMC4463808
OpenAlexW2086370314

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.