ArticleCurrent biology : CB2009
Enhanced arrestin facilitates recovery and protects rods lacking rhodopsin phosphorylation.
Article in Current biology : CB, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 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.
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
61 citing papers in PubMed, 82 citations in OpenAlex.
- The Functional Role of Gate Loop Residues in Arrestin Binding to GPCRs.International journal of molecular sciences · 2025Article
- Small angle neutron scattering study of rhodopsin oligomerization and G-protein coupling in a physiologically relevant lipid membrane.Biochimica et biophysica acta. Biomembranes · 2025Review
- The role of arrestin-1 N-edge in rhodopsin binding.Cellular signalling · 2025Article
- A small molecule enhances arrestin-3 binding to the βCommunications chemistry · 2025Article
- The Role of Individual Residues in the N-Terminus of Arrestin-1 in Rhodopsin Binding.International journal of molecular sciences · 2025Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Review
- Expression of Untagged Arrestins in E. coli and Their Purification.Current protocols · 2023Article
- The Role of Arrestin-1 Middle Loop in Rhodopsin Binding.International journal of molecular sciences · 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
- Biological Role of Arrestin-1 Oligomerization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- GPCR Signaling Regulation: The Role of GRKs and Arrestins.Frontiers in pharmacology · 2019Review
- Article
- Arrestins: structural disorder creates rich functionality.Protein & cell · 2018Review
- Molecular Defects of the Disease-Causing Human Arrestin-1 C147F Mutant.Investigative ophthalmology & visual science · 2018Article
- Arrestins: Introducing Signaling Bias Into Multifunctional Proteins.Progress in molecular biology and translational science · 2018Review
- Enhanced Mutant Compensates for Defects in Rhodopsin Phosphorylation in the Presence of Endogenous Arrestin-1.Frontiers in molecular neuroscience · 2018Article
- Molecular Mechanisms of GPCR Signaling: A Structural Perspective.International journal of molecular sciences · 2017Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) are the largest family of signaling proteins expressed in every cell in the body and are targeted by the majority of clinically used drugs [1]. GPCR signaling, including rhodopsin-driven phototransduction, is terminated by receptor phosphorylation followed by arrestin binding [2]. Genetic defects in receptor phosphorylation and excessive signaling by overactive GPCR mutants result in a wide variety of diseases, from retinal degeneration to cancer [3-6]. Here, we tested whether arrestin1 mutants with enhanced ability to bind active unphosphorylated rhodopsin [7-10] can suppress uncontrolled signaling, bypassing receptor phosphorylation by rhodopsin kinase (RK) and replacing this two-step mechanism with a single-step deactivation in rod photoreceptors. We show that in this precisely timed signaling system with single-photon sensitivity [11], an enhanced arrestin1 mutant partially compensates for defects in rhodopsin phosphorylation, promoting photoreceptor survival, improving functional performance, and facilitating photoresponse recovery. These proof-of-principle experiments demonstrate the feasibility of functional compensation in vivo for the first time, which is a promising approach for correcting genetic defects associated with gain-of-function mutations. Successful modification of protein-protein interactions by appropriate mutations paves the way to targeted redesign of signaling pathways to achieve desired functional outcomes.
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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.