ArticleFrontiers in cellular neuroscience2024
Loss of Cdc42 causes abnormal optic cup morphogenesis and microphthalmia in mouse.
Article in Frontiers in cellular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Patient-specific finite element analysis of orbital biomechanical responses to malpositioned self-inflating hydrogel implants in congenital microphthalmia.Frontiers in medicine · 2026Article
- Case Report: Association of Ocular Colobomas With a Novel Missense Variant in CDC42, a Member of the Rho Family of Small GTPases.Clinical genetics · 2025Article
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5 authors.
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Abstract
Congenital ocular malformations originate from defective morphogenesis during early eye development and cause 25% of childhood blindness. Formation of the eye is a multi-step, dynamic process; it involves evagination of the optic vesicle, followed by distal and ventral invagination, leading to the formation of a two-layered optic cup with a transient optic fissure. These tissue folding events require extensive changes in cell shape and tissue growth mediated by cytoskeleton mechanics and intercellular adhesion. We hypothesized that the Rho GTPase Cdc42 may be an essential, convergent effector downstream of key regulatory factors required for ocular morphogenesis. CDC42 controls actin remodeling, apicobasal polarity, and junction assembly. Here we identify a novel essential function for Cdc42 during eye morphogenesis in mouse; in
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