ArticleInvestigative ophthalmology & visual science2020
Heterozygous Loss of Yap1 in Mice Causes Progressive Cataracts.
Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- The Hippo signalling pathway and its impact on eye diseases.Journal of cellular and molecular medicine · 2024Pooled it
- Loss of alpha-kinase 1 contributes to the formation of congenital cataracts in mice.Cellular & molecular biology letters · 2025Article
- The protective role of quercetin in cataract lenses and its mechanisms related to the hippo signaling pathway.International ophthalmology · 2025Article
- Review
- The role of the Hippo/YAP pathway in the physiological activities and lesions of lens epithelial cells.Frontiers in cell and developmental biology · 2025Review
- Hypoxia-enhanced YAP1-EIF4A3 interaction drives circ_0007386 circularization by competing with CRIM1 pre-mRNA linear splicing and promotes non-small cell lung cancer progression.Journal of experimental & clinical cancer research : CR · 2024Article
- Uveitic glaucoma-like features in Yap conditional knockout mice.Cell death discovery · 2024Article
- Application of transgenic mice to the molecular pathogenesis of cataract.International journal of ophthalmology · 2024Review
- CELF1 Selectively Regulates Alternative Splicing of DNA Repair Genes Associated With Cataract in Human Lens Cell Line.Biochemical genetics · 2023Article
- CCN-Hippo YAP signaling in vision and its role in neuronal, glial and vascular cell function and behavior.Journal of cell communication and signaling · 2023Review
- The Hippo signalling pathway and its implications in human health and diseases.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Purpose: Yap1 encodes an evolutionarily conserved transcriptional coactivator and functions as a down-stream effector of the Hippo signaling pathway that controls tissue size and cell growth. Yap1 contributes to lens epithelial development. However, the effect of Yap1 haplodeficiency on the lens epithelium and its role in the development of cataracts has not been reported. The aim of the current study is to investigate Yap1 function and its regulatory mechanisms in lens epithelial cells (LECs). Methods: Lens phenotypes were investigated in Yap1 heterozygous mutant mice by visual observation and histological and biochemical methods. Primary LEC cultures were used to study regulatory molecular mechanism. Results: The heterozygous inactivation of Yap1 in mice caused cataracts during adulthood with defective LEC phenotypes. Despite a normal early development of the eye including the lens, the majority of Yap1 heterozygotes developed cataracts in the first six months of age. Cataract was preceded by multiple morphological defects in the lens epithelium, including decreased cell density and abnormal cell junctions. The low LEC density was coincident with reduced LEC proliferation. In addition, expression of the Yap1 target gene Crim1 was reduced in the Yap1+/- LEC, and overexpression of Crim1 restored Yap1+/- LEC cell proliferation in vitro. Conclusions: Homozygosity of the Yap1 gene was critical for adequate Crim1 expression needed to maintain the constant proliferation of LEC and to maintain a normal-sized lens. Yap1 haplodeficiency leads to cataracts.
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Registered trials
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.