ArticleThe Journal of clinical investigation2004
Structural and functional impairment of endocytic pathways by retinitis pigmentosa mutant rhodopsin-arrestin complexes.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 67 citations in OpenAlex.
- Enhanced Endocytosis and Mitochondrial Stress Underlie Severe Retinitis Pigmentosa With RHO P347L Mutant.Investigative ophthalmology & visual science · 2026Article
- NECAP antagonizes light-induced Rhodopsin-1 internalization to promote photoreceptor homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Expanding the clinical and genetic spectrum ofExperimental biology and medicine (Maywood, N.J.) · 2026Article
- P23H rhodopsin accumulation causes transient disruptions to synaptic protein levels in rod photoreceptors in a model of retinitis pigmentosa.Disease models & mechanisms · 2025Article
- Synchronized Photoactivation of T4K Rhodopsin Causes a Chromophore-Dependent Retinal Degeneration That Is Moderated by Interaction with Phototransduction Cascade Components.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Mutant mice with rod-specific VPS35 deletion exhibit retinal α-synuclein pathology-associated degeneration.Nature communications · 2024Article
- Super-resolution mapping in rod photoreceptors identifies rhodopsin trafficking through the inner segment plasma membrane as an essential subcellular pathway.PLoS biology · 2024Article
- Review
- Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.PLoS genetics · 2021Article
- Structural aspects of rod opsin and their implication in genetic diseases.Pflugers Archiv : European journal of physiology · 2021Review
- Characterizing variants of unknown significance in rhodopsin: A functional genomics approach.Human mutation · 2019Article
- A new rhodopsin R135W mutation induces endoplasmic reticulum stress and apoptosis in retinal pigment epithelial cells.Journal of cellular physiology · 2019Article
- Coupling of Human Rhodopsin to a Yeast Signaling Pathway Enables Characterization of Mutations Associated with Retinal Disease.Genetics · 2019Article
- A Small Chaperone Improves Folding and Routing of Rhodopsin Mutants Linked to Inherited Blindness.iScience · 2018Article
- Targeted disruption of the endogenous zebrafishMolecular vision · 2018Article
- The molecular and cellular basis of rhodopsin retinitis pigmentosa reveals potential strategies for therapy.Progress in retinal and eye research · 2018Review
- Aberrant protein trafficking in retinal degenerations: The initial phase of retinal remodeling.Experimental eye research · 2016Review
- Functional map of arrestin binding to phosphorylated opsin, with and without agonist.Scientific reports · 2016Article
- The Disease Protein Tulp1 Is Essential for Periactive Zone Endocytosis in Photoreceptor Ribbon Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Hsp90 as a Potential Therapeutic Target in Retinal Disease.Advances in experimental medicine and biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Retinitis pigmentosa (RP) is a clinically and genetically heterogeneous degenerative eye disease. Mutations at Arg135 of rhodopsin are associated with a severe form of autosomal dominant RP. This report presents evidence that Arg135 mutant rhodopsins (e.g., R135L, R135G, and R135W) are hyperphosphorylated and bind with high affinity to visual arrestin. Mutant rhodopsin recruits the cytosolic arrestin to the plasma membrane, and the rhodopsin-arrestin complex is internalized into the endocytic pathway. Furthermore, the rhodopsin-arrestin complexes alter the morphology of endosomal compartments and severely damage receptor-mediated endocytic functions. The biochemical and cellular defects of Arg135 mutant rhodopsins are distinct from those previously described for class I and class II RP mutations, and, hence, we propose that they be named class III. Impaired endocytic activity may underlie the pathogenesis of RP caused by class III rhodopsin mutations.
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.