Evidence map›Paper›PMID 23172727›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2013

Tissue-specific responses to aberrant FGF signaling in complex head phenotypes.

Neus Martínez-Abadías, Susan M Motch, Talia L Pankratz, Yingli Wang, Kristina Aldridge, Ethylin Wang Jabs, Joan T Richtsmeier

Open access · greenAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  12. Choanal Atresia and Craniosynostosis: Development and Disease.Plastic and reconstructive surgery · 2018
    Review
  13. Article
  14. Article
  15. Developmental and Evolutionary Significance of the Zygomatic Bone.Anatomical record (Hoboken, N.J. : 2007) · 2016
    Article
  16. Understanding craniosynostosis as a growth disorder.Wiley interdisciplinary reviews. Developmental biology · 2016
    Review
  17. Mesenchymal fibroblast growth factor receptor signaling regulates palatal shelf elevation during secondary palate formation.Developmental dynamics : an official publication of the American Association of Anatomists · 2015
    Article
  18. Article
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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

7 authors at 2 institutions in 1 country.

Neus Martínez-AbadíasDepartment of Anthropology, Pennsylvania State University, University Park, PA, USA.
Susan M Motch
Talia L Pankratz
Yingli Wang
Kristina Aldridge
Ethylin Wang Jabs
Joan T Richtsmeier
Pennsylvania State University · USUniversity of Missouri · US

Funding

Midface and Upper Airway in CraniosynostosisR01DE022988 · NIDCR · PENNSYLVANIA STATE UNIVERSITY, THE · PI JABS, ETHYLIN WANG, RICHTSMEIER, JOAN THERESE · 2012 to 2016
$3.1M
PHENOGENETICS OF SKULL AND BRAIN INTEGRATION IN CRANIOSYNOSTOSISR01DE018500 · NIDCR · PENNSYLVANIA STATE UNIVERSITY, THE · PI RICHTSMEIER, JOAN THERESE · 2008 to 2012
$2.8M
NIDCR NIH HHS 3R01DE018500-02S1NIDCR NIH HHS R01 DE018500NIDCR NIH HHS R01DE018500NIDCR NIH HHS R01 DE022988NIDCR NIH HHS R01DE022988
6 · The paper itself

Abstract

backgroundThe role of fibroblast growth factor and receptor (FGF/FGFR) signaling in bone development is well studied, partly because mutations in FGFRs cause human diseases of achondroplasia and FGFR-related craniosynostosis syndromes including Crouzon syndrome. The FGFR2c C342Y mutation is a frequent cause of Crouzon syndrome, characterized by premature cranial vault suture closure, midfacial deficiency, and neurocranial dysmorphology. Here, using newborn Fgfr2c(C342Y/+) Crouzon syndrome mice, we tested whether the phenotypic effects of this mutation go beyond the skeletal tissues of the skull, altering the development of other non-skeletal head tissues including the brain, the eyes, the nasopharynx, and the inner ears.

resultsQuantitative analysis of 3D multimodal imaging (high-resolution micro-computed tomography and magnetic resonance microscopy) revealed local differences in skull morphology and coronal suture patency between Fgfr2c(C342Y/+) mice and unaffected littermates, as well as changes in brain shape but not brain size, significant reductions in nasopharyngeal and eye volumes, and no difference in inner ear volume in Fgfr2c(C342Y/+) mice.

conclusionsThese findings provide an expanded catalogue of clinical phenotypes in Crouzon syndrome caused by aberrant FGF/FGFR signaling and evidence of the broad role for FGF/FGFR signaling in development and evolution of the vertebrate head.

Indexed as

PhenotypeAnimalsBrainCranial SuturesCraniofacial DysostosisMagnetic Resonance ImagingMiceMutation, MissenseReceptor, Fibroblast Growth Factor, Type 2Signal TransductionSkullX-Ray MicrotomographyReceptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID23172727
PMCPMC3556393
OpenAlexW1963985949

What OpenQuestion holds

Textmetadata
LicenceTDM
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.