ArticleInvestigative ophthalmology & visual science2011
Activation of unfolded protein response in transgenic mouse lenses.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Transient ER stress cell-autonomously promotes beta cell cycling in mice.Diabetologia · 2026Article
- Deficiency of Jamc Leads to Congenital Nuclear Cataract and Activates the Unfolded Protein Response in Mouse Lenses.Investigative ophthalmology & visual science · 2022Article
- A Whole-Genome RNA Interference Screen Reveals a Role forDiabetes · 2017Article
- Disassembly of the lens fiber cell nucleus to create a clear lens: The p27 descent.Experimental eye research · 2017Review
- Lens ER-stress response during cataract development in Mip-mutant mice.Biochimica et biophysica acta · 2016Article
- Unfolded-protein response-associated stabilization of p27(Cdkn1b) interferes with lens fiber cell denucleation, leading to cataract.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Ameliorative effects of SkQ1 eye drops on cataractogenesis in senescence-accelerated OXYS rats.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015Article
- Cancer Microenvironment and Endoplasmic Reticulum Stress Response.Mediators of inflammation · 2015Review
- Fine tuning of the UPR by the ubiquitin ligases Siah1/2.PLoS genetics · 2014Article
- Lens crystallin modifications and cataract in transgenic mice overexpressing acylpeptide hydrolase.The Journal of biological chemistry · 2014Article
- Functional characterization of an AQP0 missense mutation, R33C, that causes dominant congenital lens cataract, reveals impaired cell-to-cell adhesion.Experimental eye research · 2013Article
- An MIP/AQP0 mutation with impaired trafficking and function underlies an autosomal dominant congenital lamellar cataract.Experimental eye research · 2013Article
- ER stress signalling through eIF2α and CHOP, but not IRE1α, attenuates adipogenesis in mice.Diabetologia · 2013Article
- The unfolded protein response is activated in connexin 50 mutant mouse lenses.Experimental eye research · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeOverloading of unfolded or misfolded proteins in the endoplasmic reticulum (ER) can cause ER stress and activate the unfolded protein response (UPR) in the cell. The authors tested whether transgene overexpression in the mouse lens would activate the UPR.
methodsTransgenic mice expressing proteins that either enter the ER secretory pathway or are synthesized in cytosol were selected. Activation of the UPR was assessed by determining the expression levels of the ER chaperone protein BiP, the spliced form of X-box binding protein-1 (Xbp-1) mRNA, and the transcription factor CHOP. Changes in the ubiquitin-proteasome system in the mouse lens were detected by ubiquitin immunofluorescence.
resultsBiP expression was upregulated in the fiber cells of transgenic mouse lenses expressing platelet-derived growth factor-A (PDGF-A), dominant-negative fibroblast growth factor receptor (DN-FGFR), or DN-Sprouty2 (DN-Spy2). BiP upregulation occurred around embryonic day 16.5, primarily in the fiber cells adjacent to the organelle free zone. Fiber cell differentiation was disrupted in the PDGF-A and DN-Spry2 lenses, whereas the fiber cells were degenerating in the DN-FGFR lens. High levels of UPR activation and ubiquitin-labeled protein aggregates were found in the DN-FGFR lens, indicating inefficient disposal of unfolded/misfolded proteins in the fiber cells.
conclusionsThis study implies that overexpression of some transgenes in the lens can induce ER or overall cell stress in fiber cells, resulting in the activation of UPR signaling pathways. Therefore, investigators should assess the levels of UPR activation when they analyze the downstream effects of transgene expression in the lens.
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