ArticleProceedings of the National Academy of Sciences of the United States of America2013
Visual arrestin interaction with clathrin adaptor AP-2 regulates photoreceptor survival in the vertebrate retina.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- Enhanced Endocytosis and Mitochondrial Stress Underlie Severe Retinitis Pigmentosa With RHO P347L Mutant.Investigative ophthalmology & visual science · 2026Article
- PIKfyve preserves endolysosomal function in photoreceptors and RPE cells to maintain retinal integrity.Cell death & disease · 2026Article
- Article
- Protofibril Binding Peptides Recognize and Inhibit Huntingtin Amyloid FormationbioRxiv : the preprint server for biology · 2025Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Do arrestin oligomers have specific functions?Cell signaling · 2023Article
- Discrete GPCR-triggered endocytic modes enable β-arrestins to flexibly regulate cell signaling.eLife · 2022Article
- Solo vs. Chorus: Monomers and Oligomers of Arrestin Proteins.International journal of molecular sciences · 2022Review
- Arrestin Facilitates Rhodopsin DephosphorylationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Structural evidence for visual arrestin priming via complexation of phosphoinositols.Structure (London, England : 1993) · 2022Article
- Evidence of G-Protein-Coupled Receptors (GPCR) in the Parasitic ProtozoaInternational journal of molecular sciences · 2021Review
- Biological Role of Arrestin-1 Oligomerization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Dark noise and retinal degeneration from D190N-rhodopsin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- New Insights into Arrestin Recruitment to GPCRs.International journal of molecular sciences · 2020Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Activation of Rod Input in a Model of Retinal Degeneration Reverses Retinal Remodeling and Induces Formation of Functional Synapses and Recovery of Visual Signaling in the Adult Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Metabolic Deregulation of the Blood-Outer Retinal Barrier in Retinitis Pigmentosa.Cell reports · 2019Article
- The structural basis of the arrestin binding to GPCRs.Molecular and cellular endocrinology · 2019Review
- GPCR Signaling Regulation: The Role of GRKs and Arrestins.Frontiers in pharmacology · 2019Review
- Arrestins: structural disorder creates rich functionality.Protein & cell · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Arrestins bind ligand-activated, phosphorylated G protein-coupled receptors (GPCRs) and terminate the activation of G proteins. Additionally, nonvisual arrestin/GPCR complex can initiate G protein-independent intracellular signals through their ability to act as scaffolds that bring other signaling molecules to the internalized GPCR. Like nonvisual arrestins, vertebrate visual arrestin (ARR1) terminates G protein signaling from light-activated, phosphorylated GPCR, rhodopsin. Unlike nonvisual arrestins, its role as a transducer of signaling from internalized rhodopsin has not been reported in the vertebrate retina. Formation of signaling complexes with arrestins often requires recruitment of the endocytic adaptor protein, AP-2. We have previously shown that Lys296 → Glu (K296E), which is a naturally occurring rhodopsin mutation in certain humans diagnosed with autosomal dominant retinitis pigmentosa, causes toxicity through forming a stable complex with ARR1. Here we investigated whether recruitment of AP-2 by the K296E/ARR1 complex plays a role in generating the cell death signal in a transgenic mouse model of retinal degeneration. We measured the binding affinity of ARR1 for AP-2 and found that, although the affinity is much lower than that of the other arrestins, the unusually high concentration of ARR1 in rods would favor this interaction. We further demonstrate that p44, a splice variant of ARR1 that binds light-activated, phosphorylated rhodopsin but lacks the AP-2 binding motif, prevents retinal degeneration and rescues visual function in K296E mice. These results reveal a unique role of ARR1 in a G protein-independent signaling cascade in the vertebrate retina.
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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.