Evidence map›Paper›PMID 27683414›Full record

ArticleBlood2017

The EMT transcription factor Zeb2 controls adult murine hematopoietic differentiation by regulating cytokine signaling.

Jin Li, Tamara Riedt, Steven Goossens, Carmen Carrillo García, Sabrina Szczepanski, Maria Brandes, Tim Pieters, Linne Dobrosch, Ines Gütgemann, Natalie Farla and 12 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.0field-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

51 citing papers in PubMed, 71 citations in OpenAlex.

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  15. Epithelial-Mesenchymal Transition in Acute Leukemias.International journal of molecular sciences · 2024
    Review
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  17. Biomolecules · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 8 institutions in 6 countries.

Jin LiDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Tamara RiedtDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Steven GoossensInflammation Research Center, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium.
Carmen Carrillo GarcíaDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Sabrina SzczepanskiDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Maria BrandesDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Tim PietersInflammation Research Center, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium.
Linne DobroschDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Ines GütgemannDepartment of Pathology, University of Bonn, Bonn, Germany.
Natalie FarlaInflammation Research Center, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium.
Enrico RadaelliMouse and Animal Pathology Laboratory, Università degli Studi di Milano, Milan, Italy.
Paco HulpiauInflammation Research Center, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium.
Nikhil MallelaBonn-Aachen International Center for Information Technology, University of Bonn, Bonn, Germany.
Holger FröhlichBonn-Aachen International Center for Information Technology, University of Bonn, Bonn, Germany.
Roberta La StarzaDepartment of Medicine, Laboratory of Molecular Medicine, Centro Ricerche Emato-Oncologiche, University of Perugia, Perugia, Italy.
Caterina MatteucciDepartment of Medicine, Laboratory of Molecular Medicine, Centro Ricerche Emato-Oncologiche, University of Perugia, Perugia, Italy.
Tong ChenDepartment of Hematology, Huashan Hospital, Fudan University, Shanghai, China.
Peter BrossartDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
Cristina MecucciDepartment of Medicine, Laboratory of Molecular Medicine, Centro Ricerche Emato-Oncologiche, University of Perugia, Perugia, Italy.
Danny HuylebroeckLaboratory of Molecular Biology (Celgen), Department of Development and Regeneration, University of Leuven, Leuven, Belgium.
Jody J HaighAustralian Centre for Blood Diseases, Monash University, Melbourne, Australia.
Viktor JanzenDepartment of Internal Medicine III, Hematology/Oncology/Rheumatology, University of Bonn, Bonn, Germany.
University of Bonn · DEUniversity of Perugia · ITVlaams Instituut voor Biotechnologie · BEFudan University · CNGhent University · BEKU Leuven · BEMonash University · AUVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-to-mesenchymal-transition (EMT) is critical for normal embryogenesis and effective postnatal wound healing, but is also associated with cancer metastasis. SNAIL, ZEB, and TWIST families of transcription factors are key modulators of the EMT process, but their precise roles in adult hematopoietic development and homeostasis remain unclear. Here we report that genetic inactivation of Zeb2 results in increased frequency of stem and progenitor subpopulations within the bone marrow (BM) and spleen and that these changes accompany differentiation defects in multiple hematopoietic cell lineages. We found no evidence that Zeb2 is critical for hematopoietic stem cell self-renewal capacity. However, knocking out Zeb2 in the BM promoted a phenotype with several features that resemble human myeloproliferative disorders, such as BM fibrosis, splenomegaly, and extramedullary hematopoiesis. Global gene expression and intracellular signal transduction analysis revealed perturbations in specific cytokine and cytokine receptor-related signaling pathways following Zeb2 loss, especially the JAK-STAT and extracellular signal-regulated kinase pathways. Moreover, we detected some previously unknown mutations within the human Zeb2 gene (ZFX1B locus) from patients with myeloid disease. Collectively, our results demonstrate that Zeb2 controls adult hematopoietic differentiation and lineage fidelity through widespread modulation of dominant signaling pathways that may contribute to blood disorders.

Indexed as

AdultAnimalsBase SequenceBone MarrowCell DifferentiationCell LineageCytokinesEpithelial-Mesenchymal TransitionGene Expression RegulationHematopoiesis, ExtramedullaryHomeodomain ProteinsHumansJanus KinasesMiceMice, KnockoutMitogen-Activated Protein Kinase 1CytokinesHomeodomain ProteinsJanus KinasesMapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Repressor ProteinsSTAT Transcription FactorsZEB2 protein, mouseZinc Finger E-box Binding Homeobox 2

Identifiers

PMID27683414
OpenAlexW2526554341

What OpenQuestion holds

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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.