ArticleAngiogenesis2025
An endothelial specific mouse model for the capillary malformation mutation Gnaq p.R183Q.
Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed.
- From Somatic Driver to Molecular Therapy in Retinal, Choroidal and Periocular Vascular Disease: Mosaicism, Targetable Pathways and Ocular Toxicity.International journal of molecular sciences · 2026Review
- In Vitro Models of Sturge-Weber Syndrome: Strengths, Limitations, and Future Goals.International journal of molecular sciences · 2026Review
- Live imaging of vascular dynamics in mouse skin.The Journal of investigative dermatology · 2026Article
- MAPK signaling and angiopoietin-2 contribute to endothelial permeability in capillary malformations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- EndothelialFrontiers in cell and developmental biology · 2025Article
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8 authors.
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Abstract
Capillary malformation (CM) is a congenital, non-hereditary lesion composed of enlarged and tortuous blood vessels. CM is associated with a somatic p.R183Q activating mutation in the Guanine nucleotide-binding protein G(q) subunit alpha (GNAQ) gene in endothelial cells (EC). Cutaneous CMs are present in 1/300 infants and in 55-70% of CM cases soft tissue overgrowth is observed. Pharmacotherapy for CM does not exist. Here we report a conditional mouse model allowing the simultaneous tissue specific expression of GNAQ p.R183Q and Green Fluorescent Protein (GFP) from the Rosa26 (R26) locus (R26
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