Evidence map›Paper›PMID 36449606›Full record

ArticleScience advances2022

GATA3 mediates nonclassical β-catenin signaling in skeletal cell fate determination and ectopic chondrogenesis.

Takamitsu Maruyama, Daigaku Hasegawa, Tomas Valenta, Jody Haigh, Maxime Bouchard, Konrad Basler, Wei Hsu

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Disruptive innovation events in dentistry.JADA foundational science · 2024
    Article
  5. Article
  6. 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

7 authors at 5 institutions in 3 countries.

Takamitsu MaruyamaForsyth Institute, 245 First Street, Cambridge, MA 02142, USA.ORCID 0000-0001-7322-8821
Daigaku HasegawaForsyth Institute, 245 First Street, Cambridge, MA 02142, USA.ORCID 0000-0002-2593-5633
Tomas ValentaDepartment of Molecular Life Sciences, University of Zürich, CH-8057 Zürich, Switzerland.ORCID 0000-0002-3043-1835
Jody HaighCancerCare Manitoba Research Institute, Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba R3E 0V9, Canada.ORCID 0000-0002-7319-8922
Maxime BouchardGoodman Cancer Institute and Department of Biochemistry, McGill University, Montreal, Quebec H3A 1A3, Canada.
Konrad BaslerDepartment of Molecular Life Sciences, University of Zürich, CH-8057 Zürich, Switzerland.
Wei HsuForsyth Institute, 245 First Street, Cambridge, MA 02142, USA.ORCID 0000-0001-6738-6030
Life Science Zurich · CHUniversity of Rochester Medical Center · USCancerCare Manitoba · CAHarvard University · USMcGill University · CA

Funding

GENETIC REGULATORY NETWORK IN CRANIOFACIAL DEVELOPMENTR01DE015654 · NIDCR · UNIVERSITY OF ROCHESTER · PI Wei Hsu · 2006 to 2026
$8.2M
Stem cells for craniofacial bone repair and regenerationR01DE026936 · NIDCR · UNIVERSITY OF ROCHESTER · PI HSU, WEI · 2018 to 2022
$2.9M
NIDCR NIH HHS R01 DE015654NIDCR NIH HHS R01 DE026936
6 · The paper itself

Abstract

Skeletal precursors are mesenchymal in origin and can give rise to distinct sublineages. Their lineage commitment is modulated by various signaling pathways. The importance of Wnt signaling in skeletal lineage commitment has been implicated by the study of β-catenin-deficient mouse models. Ectopic chondrogenesis caused by the loss of β-catenin leads to a long-standing belief in canonical Wnt signaling that determines skeletal cell fate. As β-catenin has other functions, it remains unclear whether skeletogenic lineage commitment is solely orchestrated by canonical Wnt signaling. The study of the Wnt secretion regulator Gpr177/Wntless also raises concerns about current knowledge. Here, we show that skeletal cell fate is determined by β-catenin but independent of LEF/TCF transcription. Genomic and bioinformatic analyses further identify GATA3 as a mediator for the alternative signaling effects. GATA3 alone is sufficient to promote ectopic cartilage formation, demonstrating its essential role in mediating nonclassical β-catenin signaling in skeletogenic lineage specification.

Indexed as

beta CateninMusculoskeletal SystemAnimalsCell DifferentiationChondrogenesisGATA3 Transcription FactorMiceWnt Signaling Pathwaybeta CateninGata3 protein, mouseGATA3 Transcription Factor

Identifiers

PMID36449606
PMCPMC9710881
OpenAlexW4310599157

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.