ArticleRNA (New York, N.Y.)2008
An RNA molecule that specifically inhibits G-protein-coupled receptor kinase 2 in vitro.
Article in RNA (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 50 citations in OpenAlex.
- Recent advances in the development of GRK2 inhibitors: blocking the interaction of GRK2 with its partners.Acta pharmacologica Sinica · 2026Review
- Robotic-Assisted Capture-Systematic Evolution of Ligands by Exponential Enrichment of RNA Aptamers Binding to Small Molecules.Chembiochem : a European journal of chemical biology · 2025Article
- Therapeutic Potential of Aptamer-Protein Interactions.ACS pharmacology & translational science · 2022Review
- G protein-coupled receptor kinases as therapeutic targets in the heart.Nature reviews. Cardiology · 2019Review
- Robotic assisted generation of 2'-deoxy-2'-fluoro-modifed RNA aptamers - High performance enabling strategies in aptamer selection.Methods (San Diego, Calif.) · 2019Article
- G Protein-Coupled Receptor Kinase 2 (GRK2) as a Potential Therapeutic Target in Cardiovascular and Metabolic Diseases.Frontiers in pharmacology · 2019Review
- The Role of G Protein-coupled Receptor Kinases in Cancer.International journal of biological sciences · 2018Review
- Structure-Based Design, Synthesis, and Biological Evaluation of Highly Selective and Potent G Protein-Coupled Receptor Kinase 2 Inhibitors.Journal of medicinal chemistry · 2016Article
- Crystallographic Pursuit of a Protein-RNA Aptamer Complex.Methods in molecular biology (Clifton, N.J.) · 2016Article
- "Freeze, Don't Move": How to Arrest a Suspect in Heart Failure - A Review on Available GRK2 Inhibitors.Frontiers in cardiovascular medicine · 2016Review
- Modular Assembly of Cell-targeting Devices Based on an Uncommon G-quadruplex Aptamer.Molecular therapy. Nucleic acids · 2015Article
- Molecular basis for small molecule inhibition of G protein-coupled receptor kinases.ACS chemical biology · 2015Review
- Structural insights into G protein-coupled receptor kinase function.Current opinion in cell biology · 2014Review
- The role of HTS in drug discovery at the University of Michigan.Combinatorial chemistry & high throughput screening · 2014Review
- Article
- Stabilized Interleukin-6 receptor binding RNA aptamers.RNA biology · 2014Article
- Targeting cardiac β-adrenergic signaling via GRK2 inhibition for heart failure therapy.Frontiers in physiology · 2013Review
- d(GGGT) 4 and r(GGGU) 4 are both HIV-1 inhibitors and interleukin-6 receptor aptamers.RNA biology · 2013Article
- Paroxetine is a direct inhibitor of g protein-coupled receptor kinase 2 and increases myocardial contractility.ACS chemical biology · 2012Article
- Molecular mechanism for inhibition of g protein-coupled receptor kinase 2 by a selective RNA aptamer.Structure (London, England : 1993) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G-protein-coupled receptors are desensitized by a two-step process. In a first step, G-protein-coupled receptor kinases (GRKs) phosphorylate agonist-activated receptors that subsequently bind to a second class of proteins, the arrestins. GRKs can be classified into three subfamilies, which have been implicated in various diseases. The physiological role(s) of GRKs have been difficult to study as selective inhibitors are not available. We have used SELEX (systematic evolution of ligands by exponential enrichment) to develop RNA aptamers that potently and selectively inhibit GRK2. This process has yielded an aptamer, C13, which bound to GRK2 with a high affinity and inhibited GRK2-catalyzed rhodopsin phosphorylation with an IC50 of 4.1 nM. Phosphorylation of rhodopsin catalyzed by GRK5 was also inhibited, albeit with 20-fold lower potency (IC50 of 79 nM). Furthermore, C13 reveals significant specificity, since almost no inhibitory activity was detectable testing it against a panel of 14 other kinases. The aptamer is two orders of magnitude more potent than the best GRK2 inhibitors described previously and shows high selectivity for the GRK family of protein kinases.
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.