ArticleBMC ophthalmology2009
AlphaA-crystallin R49Cneo mutation influences the architecture of lens fiber cell membranes and causes posterior and nuclear cataracts in mice.
Article in BMC ophthalmology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Temperature and cholesterol regulate the association of native bovine lens alpha-crystallin with in vitro reconstituted membranes made of synthetically prepared lipids and cholesterol.Experimental eye research · 2026Article
- Association of Alpha-Crystallin with Human Cortical and Nuclear Lens Lipid Membrane Increases with the Grade of Cortical and Nuclear Cataract.International journal of molecular sciences · 2024Article
- Binding of Alpha-Crystallin to Cortical and Nuclear Lens Lipid Membranes Derived from a Single Lens.International journal of molecular sciences · 2022Article
- Association of Alpha-Crystallin with Fiber Cell Plasma Membrane of the Eye Lens Accompanied by Light Scattering and Cataract Formation.Membranes · 2021Review
- Cataract-causing allele in CRYAA (Y118D) proceeds through endoplasmic reticulum stress in mouse model.Zoological research · 2021Article
- Increased Association of Deamidated αA-BMC ophthalmology · 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
- Characterization of an N-terminal mutant of αA-crystallin αA-R21Q associated with congenital cataract.Experimental eye research · 2018Article
- p62 expression and autophagy in αB-crystallin R120G mutant knock-in mouse model of hereditary cataract.Experimental eye research · 2013Article
- Enhancement of ubiquitin conjugation activity reduces intracellular aggregation of V76D mutant γD-crystallin.Investigative ophthalmology & visual science · 2012Article
- Patterns of gene expression in microarrays and expressed sequence tags from normal and cataractous lenses.Human genomics · 2012Article
- Oligomerization with wt αA- and αB-crystallins reduces proteasome-mediated degradation of C-terminally truncated αA-crystallin.Investigative ophthalmology & visual science · 2012Article
- The common modification in alphaA-crystallin in the lens, N101D, is associated with increased opacity in a mouse model.The Journal of biological chemistry · 2011Article
- A knock-in mouse model for the R120G mutation of αB-crystallin recapitulates human hereditary myopathy and cataracts.PloS one · 2011Article
- Activation of the unfolded protein response by a cataract-associated αA-crystallin mutation.Biochemical and biophysical research communications · 2010Article
- Quantitative biometric phenotype analysis in mouse lenses.Molecular vision · 2010Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
backgroundAlphaA-crystallin (CRYAA/HSPB4), a major component of all vertebrate eye lenses, is a small heat shock protein responsible for maintaining lens transparency. The R49C mutation in the alphaA-crystallin protein is linked with non-syndromic, hereditary human cataracts in a four-generation Caucasian family.
methodsThis study describes a mouse cataract model generated by insertion of a neomycin-resistant (neor) gene into an intron of the gene encoding mutant R49C alphaA-crystallin. Mice carrying the neor gene and wild-type Cryaa were also generated as controls. Heterozygous knock-in mice containing one wild type gene and one mutated gene for alphaA-crystallin (WT/R49Cneo) and homozygous knock-in mice containing two mutated genes (R49Cneo/R49Cneo) were compared.
resultsBy 3 weeks, WT/R49Cneo mice exhibited large vacuoles in the cortical region 100 mum from the lens surface, and by 3 months posterior and nuclear cataracts had developed. WT/R49Cneo mice demonstrated severe posterior cataracts at 9 months of age, with considerable posterior nuclear migration evident in histological sections. R49Cneo/R49Cneo mice demonstrated nearly complete lens opacities by 5 months of age. In contrast, R49C mice in which the neor gene was deleted by breeding with CreEIIa mice developed lens abnormalities at birth, suggesting that the neor gene may suppress expression of mutant R49C alphaA-crystallin protein.
conclusionIt is apparent that modification of membrane and cell-cell interactions occurs in the presence of the alphaA-crystallin mutation and rapidly leads to lens cell pathology in vivo.
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