ArticleInvestigative ophthalmology & visual science2013
Connexin50D47A decreases levels of fiber cell connexins and impairs lens fiber cell differentiation.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- JAM-C Is Important for Lens Epithelial Cell Proliferation and Lens Fiber Maturation in Murine Lens Development.Investigative ophthalmology & visual science · 2023Article
- Patch clamp studies on TRPV4-dependent hemichannel activation in lens epithelium.Frontiers in pharmacology · 2023Article
- Levels and Modifications of Both Lens Fiber Cell Connexins Are Affected in Connexin Mutant Mice.Cells · 2022Article
- Connexin Mutations and Hereditary Diseases.International journal of molecular sciences · 2022Review
- Connexin Mutants Cause Cataracts Through Deposition of Apatite.Frontiers in cell and developmental biology · 2022Article
- Interrogation of Carboxy-Terminus LocalizedInternational journal of molecular sciences · 2022Article
- Molecular diagnosis of autosomal dominant congenital cataract in two families from North India reveals a novel and a known variant inFrontiers in pediatrics · 2022Article
- Loss of fiber cell communication may contribute to the development of cataracts of many different etiologies.Frontiers in physiology · 2022Review
- Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis.Antioxidants (Basel, Switzerland) · 2021Review
- Imbalances in the eye lens proteome are linked to cataract formation.Nature structural & molecular biology · 2021Article
- Do Connexin Mutants Cause Cataracts by Perturbing Glutathione Levels and Redox Metabolism in the Lens?Biomolecules · 2020Article
- Connexin-46/50 in a dynamic lipid environment resolved by CryoEM at 1.9 Å.Nature communications · 2020Article
- Connexin Mutants Compromise the Lens Circulation and Cause Cataracts through Biomineralization.International journal of molecular sciences · 2020Review
- p62/Sequestosome 1 levels increase and phosphorylation is altered in Cx50D47A lenses, but deletion of p62/sequestosome 1 does not improve transparency.Molecular vision · 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
- New GJA8 variants and phenotypes highlight its critical role in a broad spectrum of eye anomalies.Human genetics · 2019Article
- The Connexin50D47A Mutant Causes Cataracts by Calcium Precipitation.Investigative ophthalmology & visual science · 2019Article
- CHOP is dispensable for lens transparency in wild-type and connexin50 mutant mice.Molecular vision · 2019Article
- Chemical chaperone treatment improves levels and distributions of connexins in Cx50D47A mouse lenses.Experimental eye research · 2018Article
- Phosphorylation regulates connexin43/ZO-1 binding and release, an important step in gap junction turnover.Molecular biology of the cell · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeSubstitutions of aspartate-47 (D47) of Connexin50 (Cx50) have been linked to autosomal dominant congenital cataracts in several human pedigrees. To elucidate the lens abnormalities caused by a substitution at this position, we studied No2 mice, which carry the Cx50D47A mutation and parallel the human pathology.
methodsLenses from mice of different ages (neonatal to 4 months) were examined by dark-field and immunofluorescence microscopy. Protein levels were determined by immunoblotting using primary antibodies directed against connexins, other membrane proteins, crystallins, and proteins residing in different organelles.
resultsLenses of both heterozygous and homozygous Cx50D47A mice had cataracts and were smaller than those of wild-type littermates. Levels of Cx50 were severely reduced in mutant animals as compared with those in wild-type mice (<20% in heterozygotes and ≤3% in homozygotes). Levels of Cx46 and aquaporin0 were also decreased, but to a lesser extent. The immunostaining pattern of lens connexins was altered in mutant animals. The lenses of Cx50D47A mice showed persistence of nuclear remnants in deep regions of the lens and elevated levels of H3 histone and the mitochondrial protein, Tom20. γ-Crystallin levels were decreased in lenses of all mutant mice, and β-crystallins were reduced in homozygotes.
conclusionsThese data suggest that mice expressing Cx50D47A develop cataracts due to a severe decrease in the abundance of functional connexin channels. They also implicate Cx50 in fiber cell differentiation, since mutant lenses showed impaired degradation of organelles and decreased levels of some crystallins.
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