ArticleDisease models & mechanisms2016
Conditional deletion of AP-2β in mouse cranial neural crest results in anterior segment dysgenesis and early-onset glaucoma.
Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- Role of Neural Crest Cells in Establishing Corneal Transparency During Embryonic Development in Mice.Journal of cellular physiology · 2026Article
- Deletion of ARPKD-associated Pkhd1 gene in mice results in decreased Tfap2b expression and eye abnormalities.Nature communications · 2026Article
- Studies of mice with a large deletion of the ARPKD-associatedbioRxiv : the preprint server for biology · 2026Article
- Evaluating neural crest cell migration in a Col4a1 mutant mouse model of ocular anterior segment dysgenesis.Cells & development · 2024Article
- Transcriptional programs of Pitx2 and Tfap2a/Tfap2b controlling lineage specification of mandibular epithelium during tooth initiation.PLoS genetics · 2024Article
- TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway.Development (Cambridge, England) · 2024Article
- High-resolution genome topology of human retina uncovers super enhancer-promoter interactions at tissue-specific and multifactorial disease loci.Nature communications · 2022Article
- Zebrafish models of alx-linked frontonasal dysplasia reveal a role for Alx1 and Alx3 in the anterior segment and vasculature of the developing eye.Biology open · 2022Article
- Article
- Gene regulatory network from cranial neural crest cells to osteoblast differentiation and calvarial bone development.Cellular and molecular life sciences : CMLS · 2022Review
- Deletion of transcription factor AP-2β from the developing murine trabecular meshwork region leads to progressive glaucomatous changes.Journal of neuroscience research · 2022Article
- Co-expression of transcription factor AP-2beta (TFAP2B) and GATA3 in human mammary epithelial cells with intense, apicobasal immunoreactivity for CK8/18.Journal of molecular histology · 2021Article
- Progressive Loss of Retinal Ganglion Cells in Activating Protein-2β Neural Crest Cell Knockout Mice.Current eye research · 2021Article
- Conditional Deletion of AP-2β in the Periocular Mesenchyme of Mice Alters Corneal Epithelial Cell Fate and Stratification.International journal of molecular sciences · 2021Article
- Anomalous incisor morphology indicates tissue-specific roles for Tfap2a and Tfap2b in tooth development.Developmental biology · 2021Article
- Corneal development: Role of the periocular mesenchyme and bi-directional signaling.Experimental eye research · 2020Review
- Genetics Underlying the Interactions between Neural Crest Cells and Eye Development.Journal of developmental biology · 2020Review
- AP-2β is required for formation of the murine trabecular meshwork and Schlemm's canal.Experimental eye research · 2020Article
- The Ocular Neural Crest: Specification, Migration, and Then What?Frontiers in cell and developmental biology · 2020Review
- Localization ofThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Anterior segment dysgenesis (ASD) encompasses a group of developmental disorders in which a closed angle phenotype in the anterior chamber of the eye can occur and 50% of patients develop glaucoma. Many ASDs are thought to involve an inappropriate patterning and migration of the periocular mesenchyme (POM), which is derived from cranial neural crest cells (NCCs) and mesoderm. Although, the mechanism of this disruption is not well understood, a number of transcriptional regulatory molecules have previously been implicated in ASDs. Here, we investigate the function of the transcription factor AP-2β, encoded by Tfap2b, which is expressed in NCCs and their derivatives. Wnt1-Cre-mediated conditional deletion of Tfap2b in NCCs resulted in post-natal ocular defects typified by opacity. Histological data revealed that the conditional AP-2β NCC knockout (KO) mutants exhibited dysgenesis of multiple structures in the anterior segment of the eye including defects in the corneal endothelium, corneal stroma, ciliary body and disruption in the iridocorneal angle with adherence of the iris to the cornea. We further show that this phenotype leads to a significant increase in intraocular pressure and a subsequent loss of retinal ganglion cells and optic nerve degeneration, features indicative of glaucoma. Overall, our findings demonstrate that AP-2β is required in the POM for normal development of the anterior segment of the eye and that the AP-2β NCC KO mice might serve as a new and exciting model of ASD and glaucoma that is fully penetrant and with early post-natal onset.
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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.