ArticlePloS one2016
Frontal Bone Insufficiency in Gsk3β Mutant Mice.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- GSK3β Inhibition Ameliorates Atherosclerotic Calcification.International journal of molecular sciences · 2023Article
- METTL5 regulates cranial suture fusion via Wnt signaling.Fundamental research · 2023Article
- GSK3β Inhibition Reduced Vascular Calcification inInternational journal of molecular sciences · 2023Article
- Shifting osteogenesis in vascular calcification.JCI insight · 2021Article
- Cranial Neural Crest Cells and Their Role in the Pathogenesis of Craniofacial Anomalies and Coronal Craniosynostosis.Journal of developmental biology · 2020Review
- Finding theGenes · 2020Article
- Prickle1 regulates differentiation of frontal bone osteoblasts.Scientific reports · 2018Article
- ALK and GSK3: Shared Features of Neuroblastoma and Neural Crest Cells.Journal of experimental neuroscience · 2018Article
- Growth factor signaling alters the morphology of the zebrafish ethmoid plate.Journal of anatomy · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The development of the mammalian skull is a complex process that requires multiple tissue interactions and a balance of growth and differentiation. Disrupting this balance can lead to changes in the shape and size of skull bones, which can have serious clinical implications. For example, insufficient ossification of the bony elements leads to enlarged anterior fontanelles and reduced mechanical protection of the brain. In this report, we find that loss of Gsk3β leads to a fully penetrant reduction of frontal bone size and subsequent enlarged frontal fontanelle. In the absence of Gsk3β the frontal bone primordium undergoes increased cell death and reduced proliferation with a concomitant increase in Fgfr2-IIIc and Twist1 expression. This leads to a smaller condensation and premature differentiation. This phenotype appears to be Wnt-independent and is not rescued by decreasing the genetic dose of β-catenin/Ctnnb1. Taken together, our work defines a novel role for Gsk3β in skull development.
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Registered trials
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