ReviewCellular signalling2012
Synthetic biology with surgical precision: targeted reengineering of signaling proteins.
Review in Cellular signalling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Applications of synthetic biology in biomedicine.Molecular biomedicine · 2026Review
- A non-GPCR-binding partner interacts with a novel surface on β-arrestin1 to mediate GPCR signaling.The Journal of biological chemistry · 2020Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Structure-function analysis of β-arrestin Kurtz reveals a critical role of receptor interactions in downregulation of GPCR signaling in vivo.Developmental biology · 2019Article
- Plethora of functions packed into 45 kDa arrestins: biological implications and possible therapeutic strategies.Cellular and molecular life sciences : CMLS · 2019Review
- Arrestin-1 engineering facilitates complex stabilization with native rhodopsin.Scientific reports · 2019Article
- Structural Basis of Arrestin-Dependent Signal Transduction.Trends in biochemical sciences · 2018Review
- GPCR structure, function, drug discovery and crystallography: report from Academia-Industry International Conference (UK Royal Society) Chicheley Hall, 1-2 September 2014.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Beyond traditional pharmacology: new tools and approaches.British journal of pharmacology · 2015Review
- How genetic errors in GPCRs affect their function: Possible therapeutic strategies.Genes & diseases · 2015Article
- Analyzing the roles of multi-functional proteins in cells: The case of arrestins and GRKs.Critical reviews in biochemistry and molecular biology · 2015Review
- Mutations in arrestin-3 differentially affect binding to neuropeptide Y receptor subtypes.Cellular signalling · 2014Article
- Extensive shape shifting underlies functional versatility of arrestins.Current opinion in cell biology · 2014Review
- Arrestin-3 binds the MAP kinase JNK3α2 via multiple sites on both domains.Cellular signalling · 2014Article
- Arrestins in host-pathogen interactions.Handbook of experimental pharmacology · 2014Article
- Arrestins in apoptosis.Handbook of experimental pharmacology · 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
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
The complexity of living systems exceeds everything else studied by natural sciences. Sophisticated networks of intimately intertwined signaling pathways coordinate cellular functions. Clear understanding how the integration of multiple inputs produces coherent behavior is one of the major challenges of cell biology. Integration via perfectly timed highly regulated protein-protein interactions and precise targeting of the "output" proteins to particular substrates is emerging as a common theme of signaling regulation. This often involves specialized scaffolding proteins, whose key function is to ensure that correct partners come together in an appropriate place at the right time. Defective or faulty signaling underlies many congenital and acquired human disorders. Several pioneering studies showed that ectopic expression of existing proteins or their elements can restore functions destroyed by mutations or normalize the signaling pushed out of balance by disease and/or current small molecule-based therapy. Several recent studies show that proteins with new functional modalities can be generated by mixing and matching existing domains, or via functional recalibration and fine-tuning of existing proteins by precisely targeted mutations. Using arrestins as an example, we describe how manipulation of individual functions yields signaling-biased proteins. Creative protein redesign generates novel tools valuable for unraveling the intricacies of cell biology. Engineered proteins with specific functional changes also have huge therapeutic potential in disorders associated with inherited or acquired signaling errors.
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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.