ArticlePloS one2018
Probing the changes in gene expression due to α-crystallin mutations in mouse models of hereditary human cataract.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Transcriptome remodeling of mouse hearts during postnatal cardiac maturation and under proteotoxic stress.Molecular biology reports · 2026Article
- Identification and functional characterization of a novel CRYBB1 deletion mutation causing autosomal dominant congenital cataract in a Chinese family.BMC ophthalmology · 2026Article
- Candidate Genes for Non-Syndromic Pediatric Cataracts.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- Analysis of mouse lens morphological and proteomic abnormalities following deletion of the βB3-crystallin promoter.Experimental eye research · 2025Article
- Zebrafish as a model for crystallin-associated congenital cataracts in humans.Frontiers in cell and developmental biology · 2025Review
- A bibliometric and visualized analysis of the pathogenesis of cataracts from 1999 to 2023.Heliyon · 2024Article
- Impact of α-crystallin protein loss on zebrafish lens development.Experimental eye research · 2023Article
- Oxysterol Compounds in Mouse Mutant αA- and αB-Crystallin Lenses Can Improve the Optical Properties of the Lens.Investigative ophthalmology & visual science · 2022Article
- Imbalances in the eye lens proteome are linked to cataract formation.Nature structural & molecular biology · 2021Article
- Comprehensive Profiling of Proteome and Ubiquitome Changes in Human Lens Epithelial Cell Line after Ultraviolet-B Irradiation.ACS omega · 2020Article
- ITCH regulates oxidative stress induced by high glucose through thioredoxin interacting protein in cultured human lens epithelial cells.Molecular medicine reports · 2020Article
- Changes in relative histone abundance and heterochromatin in αA-crystallin and αB-crystallin knock-in mutant mouse lenses.BMC research notes · 2020Article
- Alpha-crystallin mutations alter lens metabolites in mouse models of human cataracts.PloS one · 2020Article
- Identification of Differential Gene Expression Pattern in Lens Epithelial Cells Derived from Cataractous and Noncataractous Lenses of Shumiya Cataract Rat.BioMed research international · 2020Article
- Lens-specific conditional knockout of Msx2 in mice leads to ocular anterior segment dysgenesis via activation of a calcium signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- RAG-Mediated DNA Breaks Attenuate PU.1 Activity in Early B Cells through Activation of a SPIC-BCLAF1 Complex.Cell reports · 2019Article
- Amyloid found in human cataracts with two-dimensional infrared spectroscopy.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Localization of αA-Crystallin in Rat Retinal Müller Glial Cells and Photoreceptors.Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada · 2018Article
- Article
- Transgenic zebrafish models reveal distinct molecular mechanisms for cataract-linked αA-crystallin mutants.PloS one · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian eye lens expresses a high concentration of crystallins (α, β and γ-crystallins) to maintain the refractive index essential for lens transparency. Crystallins are long-lived proteins that do not turnover throughout life. The structural destabilization of crystallins by UV exposure, glycation, oxidative stress and mutations in crystallin genes leads to protein aggregation and development of cataracts. Several destabilizing mutations in crystallin genes are linked with human autosomal dominant hereditary cataracts. To investigate the mechanism by which the α-crystallin mutations Cryaa-R49C and Cryab-R120G lead to cataract formation, we determined whether these mutations cause an altered expression of specific transcripts in the lens at an early postnatal age by RNA-seq analysis. Using knock-in mouse models previously generated in our laboratory, in the present work, we identified genes that exhibited altered abundance in the mutant lenses, including decreased transcripts for Clic5, an intracellular water channel in Cryaa-R49C heterozygous mutant lenses, and increased transcripts for Eno1b in Cryab-R120G heterozygous mutant lenses. In addition, RNA-seq analysis revealed increased histones H2B, H2A, and H4 gene expression in Cryaa-R49C mutant lenses, suggesting that the αA-crystallin mutation regulates histone expression via a transcriptional mechanism. Additionally, these studies confirmed the increased expression of histones H2B, H2A, and H4 by proteomic analysis of Cryaa-R49C knock-in and Cryaa;Cryab gene knockout lenses reported previously. Taken together, these findings offer additional insight into the early transcriptional changes caused by Cryaa and Cryab mutations associated with autosomal dominant human cataracts, and indicate that the transcript levels of certain genes are affected by the expression of mutant α-crystallin in vivo.
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