ArticleMolecular neurobiology2015
Robust Endoplasmic Reticulum-Associated Degradation of Rhodopsin Precedes Retinal Degeneration.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 138 citations in OpenAlex.
- Altered Retinal Dopamine Homeostasis in Murine Models of Retinitis Pigmentosa.Journal of neurochemistry · 2026Article
- WDR34 Deficiency Disrupts Retrograde Intraflagellar Transport and Induces Unfolded Protein Response-Driven Inflammation and Retinal Degeneration.Investigative ophthalmology & visual science · 2026Article
- PIKfyve preserves endolysosomal function in photoreceptors and RPE cells to maintain retinal integrity.Cell death & disease · 2026Article
- Disease mechanisms revealed in the P23H opsin knock-in mouse model of retinitis pigmentosa.PNAS nexus · 2026Article
- The P23H Rhodopsin Mouse Model Reveals a Novel Interaction Between the Endoplasmic Reticulum and Connecting Cilium Rootlet Within Photoreceptors.Investigative ophthalmology & visual science · 2026Article
- Inhibition of galanin receptor 3 slows down retina degeneration in retinitis pigmentosa through modulation of inflammatory and oxidative stress response.Scientific reports · 2026Article
- Advances in Research on Endoplasmic Reticulum-Associated Degradation Mechanisms in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2026Review
- Loss of BAP31 Is Detrimentally Aging Photoreceptors Through ER Stress-Mediated Retinal Degeneration.Cells · 2025Article
- Transcriptional downregulation of rhodopsin is associated with desensitization of rods to light-induced damage in a murine model of retinitis pigmentosa.Human molecular genetics · 2025Article
- In vivo efficacy of NRL knockdown with cell-penetrating siRNA in retinal degeneration.Scientific reports · 2025Article
- Neuroprotection of photoreceptors by combined inhibition of both Fas and autophagy pathways in P23H mice.Cell death & disease · 2025Article
- P23H rhodopsin accumulation causes transient disruptions to synaptic protein levels in rod photoreceptors in a model of retinitis pigmentosa.Disease models & mechanisms · 2025Article
- Mechanisms of photoreceptor protection upon targeting theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.bioRxiv : the preprint server for biology · 2025Article
- Article
- Less is better: various means to reduce protein load in the endoplasmic reticulum.The FEBS journal · 2025Review
- Mechanisms of Rhodopsin-Related Inherited Retinal Degeneration and Pharmacological Treatment Strategies.Cells · 2025Review
- Expanding the Clinical Spectrum ofGenes · 2024Article
- Retinal Proteome Profiling of Inherited Retinal Degeneration Across Three Different Mouse Models Suggests Common Drug Targets in Retinitis Pigmentosa.Molecular & cellular proteomics : MCP · 2024Article
- Preservation of retinal structure and function in two mouse models of inherited retinal degeneration by ONL1204, an inhibitor of the Fas receptor.Cell death & disease · 2024Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Rhodopsin is a G protein-coupled receptor essential for vision and rod photoreceptor viability. Disease-associated rhodopsin mutations, such as P23H rhodopsin, cause rhodopsin protein misfolding and trigger endoplasmic reticulum (ER) stress, activating the unfolded protein response (UPR). The pathophysiologic effects of ER stress and UPR activation on photoreceptors are unclear. Here, by examining P23H rhodopsin knock-in mice, we found that the UPR inositol-requiring enzyme 1 (IRE1) signaling pathway is strongly activated in misfolded rhodopsin-expressing photoreceptors. IRE1 significantly upregulated ER-associated protein degradation (ERAD), triggering pronounced P23H rhodopsin degradation. Rhodopsin protein loss occurred as soon as photoreceptors developed, preceding photoreceptor cell death. By contrast, IRE1 activation did not affect JNK signaling or rhodopsin mRNA levels. Interestingly, pro-apoptotic signaling from the PERK UPR pathway was also not induced. Our findings reveal that an early and significant pathophysiologic effect of ER stress in photoreceptors is the highly efficient elimination of misfolded rhodopsin protein. We propose that early disruption of rhodopsin protein homeostasis in photoreceptors could contribute to retinal degeneration.
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