ArticleHandbook of experimental pharmacology2014
Enhanced phosphorylation-independent arrestins and gene therapy.
Article in Handbook of experimental pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 11 citations in OpenAlex.
- The LPAInternational journal of molecular sciences · 2021Review
- Many faces of the GPCR-arrestin interaction.Archives of pharmacal research · 2020Review
- Uncovering missing pieces: duplication and deletion history of arrestins in deuterostomes.BMC evolutionary biology · 2017Article
- The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2017Review
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 1 institution in 1 country.
Funding
Abstract
A variety of heritable and acquired disorders is associated with excessive signaling by mutant or overstimulated GPCRs. Since any conceivable treatment of diseases caused by gain-of-function mutations requires gene transfer, one possible approach is functional compensation. Several structurally distinct forms of enhanced arrestins that bind phosphorylated and even non-phosphorylated active GPCRs with much higher affinity than parental wild-type proteins have the ability to dampen the signaling by hyperactive GPCR, pushing the balance closer to normal. In vivo this approach was so far tested only in rod photoreceptors deficient in rhodopsin phosphorylation, where enhanced arrestin improved the morphology and light sensitivity of rods, prolonged their survival, and accelerated photoresponse recovery. Considering that rods harbor the fastest, as well as the most demanding and sensitive GPCR-driven signaling cascade, even partial success of functional compensation of defect in rhodopsin phosphorylation by enhanced arrestin demonstrates the feasibility of this strategy and its therapeutic potential.
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.