Evidence map›Paper›PMID 29337667›Full record

ArticleeLife2018

Revised roles of ISL1 in a hES cell-based model of human heart chamber specification.

Roberto Quaranta, Jakob Fell, Frank Rühle, Jyoti Rao, Ilaria Piccini, Marcos J Araúzo-Bravo, Arie O Verkerk, Monika Stoll, Boris Greber

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Mechanistic insights into cardiac regeneration and protection through MEIS inhibition.Turkish journal of biology = Turk biyoloji dergisi · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Review
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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 5 institutions in 4 countries.

Roberto QuarantaHuman Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Jakob FellHuman Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Frank RühleDepartment of Genetic Epidemiology, Institute of Human Genetics, University of Münster, Münster, Germany.
Jyoti RaoHuman Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Ilaria PicciniHuman Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Marcos J Araúzo-BravoIKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
Arie O VerkerkDepartment of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.ORCID 0000-0003-2140-834X
Monika StollDepartment of Genetic Epidemiology, Institute of Human Genetics, University of Münster, Münster, Germany.
Boris GreberHuman Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-9404-7293
Max Planck Society · DEUniversity of Münster · DEAmsterdam UMC Location University of Amsterdam · NLBrigham and Women's Hospital · USIkerbasque · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor ISL1 is thought to be key for conveying the multipotent and proliferative properties of cardiac precursor cells. Here, we investigate its function upon cardiac induction of human embryonic stem cells. We find that ISL1 does not stabilize the transient cardiac precursor cell state but rather serves to accelerate cardiomyocyte differentiation. Conversely, ISL1 depletion delays cardiac differentiation and respecifies nascent cardiomyocytes from a ventricular to an atrial identity. Mechanistic analyses integrate this unrecognized anti-atrial function of ISL1 with known and newly identified atrial inducers. In this revised view, ISL1 is antagonized by retinoic acid signaling via a novel player, MEIS2. Conversely, ISL1 competes with the retinoic acid pathway for prospective cardiomyocyte fate, which converges on the atrial specifier NR2F1. This study reveals a core regulatory network putatively controlling human heart chamber formation and also bears implications for the subtype-specific production of human cardiomyocytes with enhanced functional properties.

Indexed as

Cell DifferentiationGene Expression RegulationCOUP Transcription Factor IHomeodomain ProteinsHuman Embryonic Stem CellsHumansLIM-Homeodomain ProteinsMyocytes, CardiacTranscription FactorsCOUP Transcription Factor IHomeodomain Proteinsinsulin gene enhancer binding protein Isl-1LIM-Homeodomain ProteinsMEIS2 protein, humanNR2F1 protein, humanTranscription Factorscardiac subtype specificationdevelopmental biologydirected cardiac differentiationhumanhuman embryonic stem cellsIslet-1stem cells

Identifiers

PMID29337667
PMCPMC5770158
OpenAlexW2782664696

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.