ArticleProceedings of the National Academy of Sciences of the United States of America1995
Constitutive activation of phototransduction by K296E opsin is not a cause of photoreceptor degeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 130 citations in OpenAlex.
- The oscillatory response of the electroretinogram and neuronal adaptation.Acta ophthalmologica · 2026Review
- Aggregation of the Constitutively Active K296E Rhodopsin Mutant Contributes to Retinal Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Arrestin Facilitates Rhodopsin DephosphorylationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2017Review
- Arrestins: Critical Players in Trafficking of Many GPCRs.Progress in molecular biology and translational science · 2015Review
- Photoactivation-induced instability of rhodopsin mutants T4K and T17M in rod outer segments underlies retinal degeneration in X. laevis transgenic models of retinitis pigmentosa.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Gene augmentation for adRP mutations in RHO.Cold Spring Harbor perspectives in medicine · 2014Review
- Constitutively active rhodopsin and retinal disease.Advances in pharmacology (San Diego, Calif.) · 2014Review
- Visual arrestin interaction with clathrin adaptor AP-2 regulates photoreceptor survival in the vertebrate retina.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Photoreceptor damage induced by low-intensity light: model of retinal degeneration in mammals.Molecular vision · 2013Article
- G protein-coupled receptor kinases: more than just kinases and not only for GPCRs.Pharmacology & therapeutics · 2012Review
- Rhodopsin gene expression determines rod outer segment size and rod cell resistance to a dominant-negative neurodegeneration mutant.PloS one · 2012Article
- Phenotype of transgenic mice overexpressed with inducible nitric oxide synthase in the retina.PloS one · 2012Article
- Molecular mechanisms of disease for mutations at Gly-90 in rhodopsin.The Journal of biological chemistry · 2011Article
- Beyond desensitization: physiological relevance of arrestin-dependent signaling.Pharmacological reviews · 2010Review
- Mutations of the opsin gene (Y102H and I307N) lead to light-induced degeneration of photoreceptors and constitutive activation of phototransduction in mice.The Journal of biological chemistry · 2010Article
- Female mice expressing constitutively active mutants of FSH receptor present with a phenotype of premature follicle depletion and estrogen excess.Endocrinology · 2010Article
- Effect of g protein-coupled receptor kinase 1 (Grk1) overexpression on rod photoreceptor cell viability.Investigative ophthalmology & visual science · 2010Article
- Severe retinal degeneration caused by a novel rhodopsin mutation.Investigative ophthalmology & visual science · 2010Article
- Diversity in arrestin function.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The missense mutation Lys-296-->Glu (K296E) in the rhodopsin gene produces an opsin with no chromophore binding site and therefore is not activated by light. Nevertheless, the mutant opsin constitutively activates transducin in vitro and causes photoreceptor degeneration in vivo, possibly by continuously activating the phototransduction cascade, analogous to constant exposure to environmental light. We studied the K296E mutation in eight lines of transgenic mice. Each line developed photoreceptor degeneration with the rate of degeneration increasing monotonically as the ratio of mutant:wild-type opsin mRNA increased. At no time in the course of degeneration was there endogenous light adaptation in the retina as measured by the electroretinogram. The mutant opsin was found to be invariably phosphorylated and stably bound to arrestin. Light-independent activation of transducin was demonstrated only after the removal of arrestin and dephosphorylation of K296E opsin. Thus, K296E opsin in vivo does not activate the phototransduction cascade because it is shut off by photoreceptor inactivation mechanisms. Our data show that the K296E mutation does not cause photoreceptor degeneration by continuous activation of phototransduction.
Indexed as
Identifiers
What OpenQuestion holds
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.