Evidence map›Paper›PMID 27638855›Full record

ArticleThe EMBO journal2016

Evi1 regulates Notch activation to induce zebrafish hematopoietic stem cell emergence.

Martina Konantz, Elisa Alghisi, Joëlle S Müller, Anna Lenard, Virginie Esain, Kelli J Carroll, Lothar Kanz, Trista E North, Claudia Lengerke

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Martina KonantzDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Elisa AlghisiDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Joëlle S MüllerDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Anna LenardDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Virginie EsainBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Kelli J CarrollBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Lothar KanzDepartment of Internal Medicine II, University Hospital Tuebingen, Tuebingen, Germany.
Trista E NorthBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Claudia LengerkeDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland claudia.lengerke@unibas.ch.ORCID 0000-0001-5442-2805
University Hospital of Basel · CHBeth Israel Deaconess Medical Center · US

Funding

Metabolic regulation of hematopoietic stem cell specification and functionR01DK098241 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI NORTH, TRISTA E. · 2014 to 2018
$2.0M
NIDDK NIH HHS R01 DK098241
6 · The paper itself

Abstract

During development, hematopoietic stem cells (HSCs) emerge from aortic endothelial cells (ECs) through an intermediate stage called hemogenic endothelium by a process known as endothelial-to-hematopoietic transition (EHT). While Notch signaling, including its upstream regulator Vegf, is known to regulate this process, the precise molecular control and temporal specificity of Notch activity remain unclear. Here, we identify the zebrafish transcriptional regulator evi1 as critically required for Notch-mediated EHT In vivo live imaging studies indicate that evi1 suppression impairs EC progression to hematopoietic fate and therefore HSC emergence. evi1 is expressed in ECs and induces these effects cell autonomously by activating Notch via pAKT Global or endothelial-specific induction of notch, vegf, or pAKT can restore endothelial Notch and HSC formations in evi1 morphants. Significantly, evi1 overexpression induces Notch independently of Vegf and rescues HSC numbers in embryos treated with a Vegf inhibitor. In sum, our results unravel evi1-pAKT as a novel molecular pathway that, in conjunction with the shh-vegf axis, is essential for activation of Notch signaling in VDA endothelial cells and their subsequent conversion to HSCs.

Indexed as

AnimalsAnimals, Genetically ModifiedAortaDiaminesDNA-Binding ProteinsEmbryo, NonmammalianEndothelial CellsHematopoietic Stem CellsPhosphatidylinositol 3-KinasesProto-OncogenesReceptors, NotchThiazolesTranscription FactorsVascular Endothelial Growth Factor AZebrafishZebrafish Proteins24-diamino-5-phenylthiazoleDiaminesDNA-Binding ProteinsPhosphatidylinositol 3-KinasesReceptors, NotchThiazolesTranscription FactorsVascular Endothelial Growth Factor AZebrafish ProteinsAKTendothelial‐to‐hematopoietic transitionEVI1hematopoietic stem cellsNotchVEGF

Identifiers

PMID27638855
PMCPMC5090218
OpenAlexW2519745383

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.