ReviewExpert reviews in molecular medicine2010
Custom-designed proteins as novel therapeutic tools? The case of arrestins.
Review in Expert reviews in molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 33 citations in OpenAlex.
- Modulating signalling lifetime to optimise a prototypical animal opsin for optogenetic applications.Pflugers Archiv : European journal of physiology · 2023Article
- Receptor-Arrestin Interactions: The GPCR Perspective.Biomolecules · 2021Review
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Arrestin-1 engineering facilitates complex stabilization with native rhodopsin.Scientific reports · 2019Article
- Beyond traditional pharmacology: new tools and approaches.British journal of pharmacology · 2015Review
- Mutations in arrestin-3 differentially affect binding to neuropeptide Y receptor subtypes.Cellular signalling · 2014Article
- Arrestin-3 binds the MAP kinase JNK3α2 via multiple sites on both domains.Cellular signalling · 2014Article
- Ligand- and cell-dependent determinants of internalization and cAMP modulation by delta opioid receptor (DOR) agonists.Cellular and molecular life sciences : CMLS · 2014Article
- Therapeutic potential of small molecules and engineered proteins.Handbook of experimental pharmacology · 2014Article
- Constitutively active rhodopsin mutants causing night blindness are effectively phosphorylated by GRKs but differ in arrestin-1 binding.Cellular signalling · 2013Article
- Critical role of the central 139-loop in stability and binding selectivity of arrestin-1.The Journal of biological chemistry · 2013Article
- Engineering visual arrestin-1 with special functional characteristics.The Journal of biological chemistry · 2013Article
- Structural determinants of arrestin functions.Progress in molecular biology and translational science · 2013Review
- A non-stop S-antigen gene mutation is associated with late onset hereditary retinal degeneration in dogs.Molecular vision · 2013Article
- Conformation of receptor-bound visual arrestin.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Synthetic biology with surgical precision: targeted reengineering of signaling proteins.Cellular signalling · 2012Review
- Manipulation of very few receptor discriminator residues greatly enhances receptor specificity of non-visual arrestins.The Journal of biological chemistry · 2012Article
- Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 activity in cell by dominant-negative arrestin-3 mutant.The Journal of biological chemistry · 2012Article
- Role of receptor-attached phosphates in binding of visual and non-visual arrestins to G protein-coupled receptors.The Journal of biological chemistry · 2012Article
- Nonvisual arrestins function as simple scaffolds assembling the MKK4-JNK3α2 signaling complex.Biochemistry · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multiple genetic disorders can be associated with excessive signalling by mutant G-protein-coupled receptors (GPCRs) that are either constitutively active or have lost sites where phosphorylation by GPCR kinases is necessary for desensitisation by cognate arrestins. Phosphorylation-independent arrestin1 can compensate for defects in phosphorylation of the GPCR rhodopsin in retinal rod cells, facilitating recovery, improving light responsiveness, and promoting photoreceptor survival. These proof-of-principle experiments show that, based on mechanistic understanding of the inner workings of a protein, one can modify its functional characteristics to generate custom-designed mutants that improve the balance of signalling in congenital and acquired disorders. Manipulations of arrestin elements responsible for scaffolding mitogen-activated protein kinase cascades and binding other signalling proteins involved in life-or-death decisions in the cell are likely to yield mutants that affect cell survival and proliferation in the desired direction. Although this approach is still in its infancy, targeted redesign of individual functions of many proteins offers a promise of a completely new therapeutic toolbox with huge 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.