Evidence map›Paper›PMID 24585688›Full record

ArticleStem cells (Dayton, Ohio)2014

Hhex and Cer1 mediate the Sox17 pathway for cardiac mesoderm formation in embryonic stem cells.

Yu Liu, Ruri Kaneda, Thomas W Leja, Tatiana Subkhankulova, Oleg Tolmachov, Gabriella Minchiotti, Robert J Schwartz, Mauricio Barahona, Michael D Schneider

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. SOX17 in pulmonary arterial hypertension: from development to clinical phenotype.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  3. Article
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  15. miR-322/-503 cluster is expressed in the earliest cardiac progenitor cells and drives cardiomyocyte specification.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Article
  17. Article
  18. Genetic networks governing heart development.Cold Spring Harbor perspectives in medicine · 2014
    Review
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 3 countries.

Yu LiuCenter for Cardiovascular Development, Baylor College of Medicine, Houston, Texas, USA; Institute for Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas, USA.
Ruri Kaneda
Thomas W Leja
Tatiana Subkhankulova
Oleg Tolmachov
Gabriella Minchiotti
Robert J Schwartz
Mauricio Barahona
Michael D Schneider
British Heart Foundation · GBBaylor College of Medicine · USTexas A&M University · USImperial College London · GBInstitute of Genetics and Biophysics · IT

Funding

UNDERSTANDING OUTFLOW TRACT DEFECTS IN DIGEORGE SYNDROME--CHROMOSOME ENGINEERINGP01HL049953 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI SCHNEIDER, MICHAEL J · 1993 to 2007
$16.3M
British Heart Foundation CH/08/002British Heart Foundation RE/08/002British Heart Foundation RG/08/007/25296Medical Research Council G0901467NHLBI NIH HHS P01 HL049953NHLBI NIH HHS P01 HL49953
6 · The paper itself

Abstract

Cardiac muscle differentiation in vivo is guided by sequential growth factor signals, including endoderm-derived diffusible factors, impinging on cardiogenic genes in the developing mesoderm. Previously, by RNA interference in AB2.2 mouse embryonic stem cells (mESCs), we identified the endodermal transcription factor Sox17 as essential for Mesp1 induction in primitive mesoderm and subsequent cardiac muscle differentiation. However, downstream effectors of Sox17 remained to be proven functionally. In this study, we used genome-wide profiling of Sox17-dependent genes in AB2.2 cells, RNA interference, chromatin immunoprecipitation, and luciferase reporter genes to dissect this pathway. Sox17 was required not only for Hhex (a second endodermal transcription factor) but also for Cer1, a growth factor inhibitor from endoderm that, like Hhex, controls mesoderm patterning in Xenopus toward a cardiac fate. Suppressing Hhex or Cer1 blocked cardiac myogenesis, although at a later stage than induction of Mesp1/2. Hhex was required but not sufficient for Cer1 expression. Over-expression of Sox17 induced endogenous Cer1 and sequence-specific transcription of a Cer1 reporter gene. Forced expression of Cer1 was sufficient to rescue cardiac differentiation in Hhex-deficient cells. Thus, Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis in mESCs, acting at a stage downstream from Mesp1/2.

Indexed as

Signal TransductionAnimalsBinding SitesBody PatterningCell DifferentiationCytokinesEmbryonic Stem CellsGene Expression ProfilingGene Expression Regulation, DevelopmentalGenomeHMGB ProteinsHomeodomain ProteinsInhibin-beta SubunitsMesodermMiceModels, BiologicalCer1 protein, mouseCytokinesHhex protein, mouseHMGB ProteinsHomeodomain Proteinsinhibin beta A subunitInhibin-beta SubunitsNodal ProteinNodal protein, mouseProteinsSox17 protein, mouseSOXF Transcription FactorsTranscription FactorsCardiac developmentEmbryonic stem cellsEndodermMyogenesisRNA interference

Identifiers

PMID24585688
PMCPMC4260090
OpenAlexW1601840771

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.