ArticleThe Journal of biological chemistry2013
Insulin receptor signaling in cones.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- PIKfyve preserves endolysosomal function in photoreceptors and RPE cells to maintain retinal integrity.Cell death & disease · 2026Article
- Local Insulin for Local Needs? Insights into Retinal Insulin Signaling and RPE Metabolism.Biomolecules · 2025Review
- Real world pharmacovigilance assessment of drug related macular degeneration risks.Scientific reports · 2025Article
- The function of lactate dehydrogenase A in retinal neurons: implications to retinal degenerative diseases.PNAS nexus · 2023Article
- Increased intravitreal glucose in rhegmatogenous retinal detachment.Eye (London, England) · 2023Article
- Proteomic Profiling Revealed Mitochondrial Dysfunction in Photoreceptor Cells under Hyperglycemia.International journal of molecular sciences · 2022Article
- Insulin-like growth factor 1 receptor mediates photoreceptor neuroprotection.Cell death & disease · 2022Article
- Photoreceptor cells and RPE contribute to the development of diabetic retinopathy.Progress in retinal and eye research · 2021Review
- Diabetic Retinopathy and Insulin Insufficiency: Beta Cell Replacement as a Strategy to Prevent Blindness.Frontiers in endocrinology · 2021Article
- Insulin inhibits inflammation-induced cone death in retinal detachment.Journal of neuroinflammation · 2020Article
- Article
- A non-canonical rhodopsin-mediated insulin receptor signaling pathway in retinal photoreceptor neurons.Cell biology international · 2020Article
- Structural but Not Functional Alterations in Cones in the Absence of the Retinal Disease Protein Retinitis Pigmentosa 2 (RP2) in a Cone-Only Retina.Frontiers in genetics · 2019Article
- The Prohormone Proinsulin as a Neuroprotective Factor: Past History and Future Prospects.Frontiers in molecular neuroscience · 2018Review
- Metabolic and redox signaling in the retina.Cellular and molecular life sciences : CMLS · 2017Review
- Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats.Scientific reports · 2017Article
- The Warburg Effect Mediator Pyruvate Kinase M2 Expression and Regulation in the Retina.Scientific reports · 2016Article
- Activation of oncogenic tyrosine kinase signaling promotes insulin receptor-mediated cone photoreceptor survival.Oncotarget · 2016Article
- Loss of human disease protein retinitis pigmentosa GTPase regulator (RPGR) differentially affects rod or cone-enriched retina.Human molecular genetics · 2016Article
- Arrestin 1 and Cone Arrestin 4 Have Unique Roles in Visual Function in an All-Cone Mouse Retina.Investigative ophthalmology & visual science · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
In humans, age-related macular degeneration and diabetic retinopathy are the most common disorders affecting cones. In retinitis pigmentosa (RP), cone cell death precedes rod cell death. Systemic administration of insulin delays the death of cones in RP mouse models lacking rods. To date there are no studies on the insulin receptor signaling in cones; however, mRNA levels of IR signaling proteins are significantly higher in cone-dominant neural retina leucine zipper (Nrl) knock-out mouse retinas compared with wild type rod-dominant retinas. We previously reported that conditional deletion of the p85α subunit of phosphoinositide 3-kinase (PI3K) in cones resulted in age-related cone degeneration, and the phenotype was not rescued by healthy rods, raising the question of why cones are not protected by the rod-derived cone survival factors. Interestingly, systemic administration of insulin has been shown to delay the death of cones in mouse models of RP lacking rods. These observations led to the hypothesis that cones may have their own endogenous neuroprotective pathway, or rod-derived cone survival factors may be signaled through cone PI3K. To test this hypothesis we generated p85α(-/-)/Nrl(-/-) double knock-out mice and also rhodopsin mutant mice lacking p85α and examined the effect of the p85α subunit of PI3K on cone survival. We found that the rate of cone degeneration is significantly faster in both of these models compared with respective mice with competent p85α. These studies suggest that cones may have their own endogenous PI3K-mediated neuroprotective pathway in addition to the cone viability survival signals derived from rods.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.