ArticleCellular signalling2013
Rapid degeneration of rod photoreceptors expressing self-association-deficient arrestin-1 mutant.
Article in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Structure and self-association of Arrestin-1.Journal of structural biology · 2025Review
- Insights into the Activation and Self-Association of Arrestin-1.Biochemistry · 2025Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Modulating signalling lifetime to optimise a prototypical animal opsin for optogenetic applications.Pflugers Archiv : European journal of physiology · 2023Article
- Expression of Untagged Arrestins in E. coli and Their Purification.Current protocols · 2023Article
- Solo vs. Chorus: Monomers and Oligomers of Arrestin Proteins.International journal of molecular sciences · 2022Review
- Biological Role of Arrestin-1 Oligomerization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Phosphorylated peptide of G protein-coupled receptor induces dimerization in activated arrestin.Scientific reports · 2020Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Requirements for Neurogenin2 during mouse postnatal retinal neurogenesis.Developmental biology · 2018Article
- Rhythmic Regulation of Photoreceptor and RPE Genes Important for Vision and Genetically Associated With Severe Retinal Diseases.Investigative ophthalmology & visual science · 2018Article
- Enhanced Mutant Compensates for Defects in Rhodopsin Phosphorylation in the Presence of Endogenous Arrestin-1.Frontiers in molecular neuroscience · 2018Article
- Molecular Defects of the Disease-Causing Human Arrestin-1 C147F Mutant.Investigative ophthalmology & visual science · 2018Article
- Differential manipulation of arrestin-3 binding to basal and agonist-activated G protein-coupled receptors.Cellular signalling · 2017Article
- The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2017Review
- Beyond traditional pharmacology: new tools and approaches.British journal of pharmacology · 2015Review
- Analyzing the roles of multi-functional proteins in cells: The case of arrestins and GRKs.Critical reviews in biochemistry and molecular biology · 2015Review
- Self-association of arrestin family members.Handbook of experimental pharmacology · 2014Article
- Arrestins in apoptosis.Handbook of experimental pharmacology · 2014Article
- Enhanced phosphorylation-independent arrestins and gene therapy.Handbook of experimental pharmacology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Arrestin-1 binds light-activated phosphorhodopsin and ensures timely signal shutoff. We show that high transgenic expression of an arrestin-1 mutant with enhanced rhodopsin binding and impaired oligomerization causes apoptotic rod death in mice. Dark rearing does not prevent mutant-induced cell death, ruling out the role of arrestin complexes with light-activated rhodopsin. Similar expression of WT arrestin-1 that robustly oligomerizes, which leads to only modest increase in the monomer concentration, does not affect rod survival. Moreover, WT arrestin-1 co-expressed with the mutant delays retinal degeneration. Thus, arrestin-1 mutant directly affects cell survival via binding partner(s) other than light-activated rhodopsin. Due to impaired self-association of the mutant its high expression dramatically increases the concentration of the monomer. The data suggest that monomeric arrestin-1 is cytotoxic and WT arrestin-1 protects rods by forming mixed oligomers with the mutant and/or competing with it for the binding to non-receptor partners. Thus, arrestin-1 self-association likely serves to keep low concentration of the toxic monomer. The reduction of the concentration of harmful monomer is an earlier unappreciated biological function of protein oligomerization.
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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.