Evidence map›Paper›PMID 28186500›Full record

ArticleCell death and differentiation2017

EVI2B is a C/EBPα target gene required for granulocytic differentiation and functionality of hematopoietic progenitors.

Polina Zjablovskaja, Miroslava Kardosova, Petr Danek, Pavla Angelisova, Touati Benoukraf, Alexander A Wurm, Tomas Kalina, Stephanie Sian, Martin Balastik, Ruud Delwel and 7 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 10 institutions in 6 countries.

Polina ZjablovskajaDepartment of Hemato-oncology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20 Prague 4, Czech Republic.
Miroslava KardosovaDepartment of Hemato-oncology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20 Prague 4, Czech Republic.
Petr DanekDepartment of Hemato-oncology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20 Prague 4, Czech Republic.
Pavla AngelisovaDepartment of Molecular Immunology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20, Czech Republic.
Touati BenoukrafCancer Science Institute, National University of Singapore, 14 Medical Drive, Singapore 117599, Singapore.
Alexander A WurmDivision of Hematology and Oncology, Leipzig University Hospital, Leipzig, Germany.
Tomas KalinaChildhood Leukaemia Investigation Prague, Department of Paediatric Haematology and Oncology, 2nd Faculty of Medicine, Charles University in Prague, University Hospital Motol, V Uvalu 84, Praha 150 06, Czech Republic.
Stephanie SianCancer Science Institute, National University of Singapore, 14 Medical Drive, Singapore 117599, Singapore.
Martin BalastikDepartment of Molecular Neurobiology, Institute of Physiology of the ASCR, Videnska 1083, Prague 142 20, Czech Republic.
Ruud DelwelDepartment of Hematology, Erasmus University Medical Center, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands.
Tomas BrdickaDepartment of Leukocyte Signalling, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20, Czech Republic.
Daniel G TenenCancer Science Institute, National University of Singapore, 14 Medical Drive, Singapore 117599, Singapore.
Gerhard BehreDivision of Hematology and Oncology, Leipzig University Hospital, Leipzig, Germany.
Fréderic FioreCentre d'Immunophénomique, Aix Marseille Université, Inserm, CNRS, Marseille F-13288, France.
Bernard MalissenCentre d'Immunologie de Marseille-Luminy, Aix Marseille Université, Inserm, CNRS, Marseille F-13288, France.
Vaclav HorejsiDepartment of Molecular Immunology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20, Czech Republic.
Meritxell Alberich-JordaDepartment of Hemato-oncology, Institute of Molecular Genetics of the ASCR, Videnska 1083, Prague 142 20 Prague 4, Czech Republic.
Czech Academy of Sciences, Institute of Molecular Genetics · CZLeipzig University · DENational University of Singapore · SGCentre National de la Recherche Scientifique · FRCharles University · CZErasmus MC · NLInserm · FRInstitute of Microbiology · BYNational University Cancer Institute, Singapore · SGUniversity Hospital in Motol · CZ

Funding

Transcriptional and epigenetic heterogeneity of stem/progenitor cellsP01HL131477 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David T Scadden · 2017 to 2026
$24.6M
Mechanisms of regulation by RNA in acute myeloid leukemiaR35CA197697 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2015 to 2021
$7.1M
NCI NIH HHS R35 CA197697NHLBI NIH HHS P01 HL131477
6 · The paper itself

Abstract

Development of hematopoietic populations through the process of differentiation is critical for proper hematopoiesis. The transcription factor CCAAT/enhancer binding protein alpha (C/EBPα) is a master regulator of myeloid differentiation, and the identification of C/EBPα target genes is key to understand this process. Here we identified the Ecotropic Viral Integration Site 2B (EVI2B) gene as a direct target of C/EBPα. We showed that the product of the gene, the transmembrane glycoprotein EVI2B (CD361), is abundantly expressed on the surface of primary hematopoietic cells, the highest levels of expression being reached in mature granulocytes. Using shRNA-mediated downregulation of EVI2B in human and murine cell lines and in primary hematopoietic stem and progenitor cells, we demonstrated impaired myeloid lineage development and altered progenitor functions in EVI2B-silenced cells. We showed that the compromised progenitor functionality in Evi2b-depleted cells can be in part explained by deregulation of cell proliferation and apoptosis. In addition, we generated an Evi2b knockout murine model and demonstrated altered properties of hematopoietic progenitors, as well as impaired G-CSF dependent myeloid colony formation in the knockout cells. Remarkably, we found that EVI2B is significantly downregulated in human acute myeloid leukemia samples characterized by defects in CEBPA. Altogether, our data demonstrate that EVI2B is a downstream target of C/EBPα, which regulates myeloid differentiation and functionality of hematopoietic progenitors.

Indexed as

AnimalsApoptosisBone Marrow CellsCCAAT-Enhancer-Binding Protein-alphaCell DifferentiationCell ProliferationCells, CulturedDown-RegulationEstradiolGranulocyte Colony-Stimulating FactorGranulocytesHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMembrane GlycoproteinsMembrane ProteinsCCAAT-Enhancer-Binding Protein-alphaEstradiolEVI2B protein, humanGranulocyte Colony-Stimulating FactorMembrane GlycoproteinsMembrane ProteinsRNA, Small Interfering

Identifiers

PMID28186500
PMCPMC5384033
OpenAlexW2587736822

What OpenQuestion holds

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Registered trials

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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.