ArticlePloS one2019
Critical role of the finger loop in arrestin binding to the receptors.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular mechanism of β-arrestin 2 interaction with phosphorylated intracellular loop 3 of dopamine receptor D2.Communications biology · 2025Article
- Functional Role of Arrestin-1 Residues Interacting with Unphosphorylated Rhodopsin Elements.International journal of molecular sciences · 2023Article
- Structural Basis of Arrestin Selectivity for Active Phosphorylated G Protein-Coupled Receptors.International journal of molecular sciences · 2021Review
- The finger loop as an activation sensor in arrestin.Journal of neurochemistry · 2021Article
- Receptor-Arrestin Interactions: The GPCR Perspective.Biomolecules · 2021Review
- Lysine in the lariat loop of arrestins does not serve as phosphate sensor.Journal of neurochemistry · 2021Article
- The single nucleotide β -arrestin2 variant, A248T, resembles dynamical properties of activated arrestin.Turkish journal of chemistry · 2020Article
- Plethora of functions packed into 45 kDa arrestins: biological implications and possible therapeutic strategies.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We tested the interactions with four different G protein-coupled receptors (GPCRs) of arrestin-3 mutants with substitutions in the four loops, three of which contact the receptor in the structure of the arrestin-1-rhodopsin complex. Point mutations in the loop at the distal tip of the N-domain (Glu157Ala), in the C-loop (Phe255Ala), back loop (Lys313Ala), and one of the mutations in the finger loop (Gly65Pro) had mild variable effects on receptor binding. In contrast, the deletion of Gly65 at the beginning of the finger loop reduced the binding to all GPCRs tested, with the binding to dopamine D2 receptor being affected most dramatically. Thus, the presence of a glycine at the beginning of the finger loop appears to be critical for the arrestin-receptor interaction.
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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.