Evidence map›Paper›PMID 26204127›Full record

ArticleNature communications2015

Repression of arterial genes in hemogenic endothelium is sufficient for haematopoietic fate acquisition.

Carlos O Lizama, John S Hawkins, Christopher E Schmitt, Frank L Bos, Joan P Zape, Kelly M Cautivo, Hugo Borges Pinto, Alexander M Rhyner, Hui Yu, Mary E Donohoe and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
–field-weighted citation impact
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

88 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Jund orchestratesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. NMolecular medicine (Cambridge, Mass.) · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. The evolving hematopoietic niche during development.Frontiers in molecular biosciences · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Article

28 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

12 authors.

Carlos O LizamaCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
John S HawkinsCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
Christopher E SchmittCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
Frank L BosCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
Joan P ZapeCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
Kelly M CautivoDepartment of Nutrition, Diabetes, and Metabolism, School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile.
Hugo Borges PintoBurke Medical Research Institute, White Plains, New York 10605, USA.
Alexander M RhynerDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA.
Hui YuCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.
Mary E DonohoeBurke Medical Research Institute, White Plains, New York 10605, USA.
Joshua D WytheDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA.
Ann C ZoveinCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94158, USA.

Funding

PREDOCTORAL TRAINING IN BIOMEDICAL SCIENCEST32GM008568 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANSEL, KARL MARK · 1995 to 2019
$6.3M
Engineering human endothelium for hematopoietic stem cell productionDP2HL117743 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZOVEIN, ANN CAPELA · 2012 to 2012
$2.4M
NHLBI NIH HHS DP2 HL117743NIGMS NIH HHS T32 GM008568Wellcome Trust
6 · The paper itself

Abstract

Changes in cell fate and identity are essential for endothelial-to-haematopoietic transition (EHT), an embryonic process that generates the first adult populations of haematopoietic stem cells (HSCs) from hemogenic endothelial cells. Dissecting EHT regulation is a critical step towards the production of in vitro derived HSCs. Yet, we do not know how distinct endothelial and haematopoietic fates are parsed during the transition. Here we show that genes required for arterial identity function later to repress haematopoietic fate. Tissue-specific, temporally controlled, genetic loss of arterial genes (Sox17 and Notch1) during EHT results in increased production of haematopoietic cells due to loss of Sox17-mediated repression of haematopoietic transcription factors (Runx1 and Gata2). However, the increase in EHT can be abrogated by increased Notch signalling. These findings demonstrate that the endothelial haematopoietic fate switch is actively repressed in a population of endothelial cells, and that derepression of these programs augments haematopoietic output.

Indexed as

AnimalsBlood VesselsCore Binding Factor Alpha 2 SubunitFemaleGATA2 Transcription FactorGenes, ReporterHemangioblastsHematopoiesisHMGB ProteinsMicePregnancyReceptor, Notch1SOXF Transcription FactorsCore Binding Factor Alpha 2 SubunitGata2 protein, mouseGATA2 Transcription FactorHMGB ProteinsNotch1 protein, mouseReceptor, Notch1Runx1 protein, mouseSox17 protein, mouseSOXF Transcription Factors

Identifiers

PMID26204127
PMCPMC4519987

What OpenQuestion holds

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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.