ArticleThe Journal of biological chemistry2016
The Cataract-linked Mutant Connexin50D47A Causes Endoplasmic Reticulum Stress in Mouse Lenses.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Hypoxia Increases Connexin46 and Connexin43 Levels in KNS-42 Glioblastoma Cells.International journal of molecular sciences · 2026Article
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- JAM-C Is Important for Lens Epithelial Cell Proliferation and Lens Fiber Maturation in Murine Lens Development.Investigative ophthalmology & visual science · 2023Article
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Endoplasmic Reticulum Stress and the Lysosomal Pathway Play Crucial Roles in the Progression of βB2-Crystallin Mutation-Induced Congenital Cataracts in Mice.Investigative ophthalmology & visual science · 2023Article
- Article
- Levels and Modifications of Both Lens Fiber Cell Connexins Are Affected in Connexin Mutant Mice.Cells · 2022Article
- Cellular mechanisms of connexin-based inherited diseases.Trends in cell biology · 2022Review
- Molecular mechanisms underlying enhanced hemichannel function of a cataract-associated Cx50 mutant.Biophysical journal · 2021Article
- Inherited cataracts: Genetic mechanisms and pathways new and old.Experimental eye research · 2021Review
- Curcumin Metabolite Tetrahydrocurcumin in the Treatment of Eye Diseases.International journal of molecular sciences · 2020Review
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
- Do Connexin Mutants Cause Cataracts by Perturbing Glutathione Levels and Redox Metabolism in the Lens?Biomolecules · 2020Article
- Alleviating chronic ER stress by p38-Ire1-Xbp1 pathway and insulin-associated autophagy in C. elegans neurons.PLoS genetics · 2020Article
- Connexin 50-R205G Mutation Perturbs Lens Epithelial Cell Proliferation and Differentiation.Investigative ophthalmology & visual science · 2020Article
- 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
- GJA8 missense mutation disrupts hemichannels and induces cell apoptosis in human lens epithelial cells.Scientific reports · 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
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mice expressing connexin50D47A (Cx50D47A) exhibit nuclear cataracts and impaired differentiation. Cx50D47A does not traffic properly, and homozygous mutant lenses show increased levels of the stress-responsive αB-crystallins. Therefore, we assessed whether expression of Cx50D47A led to endoplasmic reticulum (ER) stress in the lens in vivo Although pharmacologic induction of ER stress can be transduced by three different pathways, we found no evidence for activation of the IRE1α or ATF6 pathways in Cx50D47A-expressing lenses. In contrast, heterozygous and homozygous Cx50D47A lenses showed an increase in phosphorylated PERK immunoreactivity and in the ratio of phosphorylated to total EIF2α (2.4- and 3.3-fold, respectively) compared with wild type. Levels of ATF4 were similar in wild type and heterozygous lenses but elevated in homozygotes (391%). In both heterozygotes and homozygotes, levels of calreticulin protein were increased (184 and 262%, respectively), as was Chop mRNA (1.9- and 12.4-fold, respectively). CHOP protein was increased in homozygotes (384%). TUNEL staining was increased in Cx50D47A lenses, especially in homozygous mice. Levels of two factors that may be pro-survival, Irs2 and Trib3, were greatly increased in homozygous lenses. These results suggest that expression of Cx50D47A induces ER stress, triggering activation of the PERK-ATF4 pathway, which potentially contributes to the lens pathology and leads to increased expression of anti-apoptotic factors, allowing cell survival.
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