Evidence map›Paper›PMID 28604778›Full record

ArticlePLoS genetics2017

p63 exerts spatio-temporal control of palatal epithelial cell fate to prevent cleft palate.

Rose Richardson, Karen Mitchell, Nigel L Hammond, Maria Rosaria Mollo, Evelyn N Kouwenhoven, Niki D Wyatt, Ian J Donaldson, Leo Zeef, Tim Burgis, Rognvald Blance and 8 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. The role of Rho GTPases in facial morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
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  8. Functional analysis ofbioRxiv : the preprint server for biology · 2024
    Article
  9. Context dependent activity of p63-bound gene regulatory elements.bioRxiv : the preprint server for biology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Canonical Wnt signaling is not required forFrontiers in physiology · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

18 authors at 4 institutions in 4 countries.

Rose RichardsonFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Karen MitchellFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Nigel L HammondFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Maria Rosaria MolloCEINGE Biotecnologie Avanzate Scarl (Center for Genetic Engineering), Napoli, Italy.
Evelyn N KouwenhovenDepartment of Molecular Developmental Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.
Niki D WyattFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Ian J DonaldsonFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Leo ZeefFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Tim BurgisFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Rognvald BlanceFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Simon J van HeeringenDepartment of Molecular Developmental Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.ORCID http://orcid.org/0000-0002-0411-3219
Hendrik G StunnenbergDepartment of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.
Huiqing ZhouDepartment of Molecular Developmental Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.
Caterina MisseroCEINGE Biotecnologie Avanzate Scarl (Center for Genetic Engineering), Napoli, Italy.
Rose Anne RomanoDepartment of Oral Biology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, New York, United States of America.
Satrajit SinhaDepartment of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, United States of America.
Michael J DixonFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
Jill DixonFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.ORCID http://orcid.org/0000-0001-9774-7095
Manchester Academic Health Science Centre · GBRadboud University Nijmegen · NLCeinge Biotecnologie Avanzate (Italy) · ITUniversity at Buffalo, State University of New York · US

Funding

Medical Research Council G0901539Medical Research Council MR/M012174/1
6 · The paper itself

Abstract

Cleft palate is a common congenital disorder that affects up to 1 in 2500 live births and results in considerable morbidity to affected individuals and their families. The aetiology of cleft palate is complex with both genetic and environmental factors implicated. Mutations in the transcription factor p63 are one of the major individual causes of cleft palate; however, the gene regulatory networks in which p63 functions remain only partially characterized. Our findings demonstrate that p63 functions as an essential regulatory molecule in the spatio-temporal control of palatal epithelial cell fate to ensure appropriate fusion of the palatal shelves. Initially, p63 induces periderm formation and controls its subsequent maintenance to prevent premature adhesion between adhesion-competent, intra-oral epithelia. Subsequently, TGFβ3-induced down-regulation of p63 in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate.

Indexed as

AnimalsCell MovementCell ProliferationCleft PalateDisease Models, AnimalEpithelial CellsGene Expression Regulation, DevelopmentalGene Regulatory NetworksHumansMiceMutationPhosphoproteinsSignal TransductionTrans-ActivatorsTransforming Growth Factor beta3PhosphoproteinsTgfb3 protein, mouseTrans-ActivatorsTransforming Growth Factor beta3Trp63 protein, mouse

Identifiers

PMID28604778
PMCPMC5484519
OpenAlexW2626234955

What OpenQuestion holds

Textmetadata
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.