ArticleCurrent neuropharmacology2007
Allosteric theory: taking therapeutic advantage of the malleable nature of GPCRs.
Article in Current neuropharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Efficient Characterization of GPCRs Allosteric Modulation: Application to the Rational Design of De Novo S1PR1 Allosteric Modulators.Journal of chemical information and modeling · 2025Article
- Article
- Review
- Determination of the Cannabinoid CB1 Receptor's Positive Allosteric Modulator Binding Site through Mutagenesis Studies.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Brain Structure and Function: Insights from Chemical Neuroanatomy.Life (Basel, Switzerland) · 2023Article
- In Vitro Characterization of 6-Methyl-3-(2-nitro-1-(thiophen-2-yl)ethyl)-2-phenyl-1ACS pharmacology & translational science · 2022Article
- G protein signaling-biased mu opioid receptor agonists that produce sustained G protein activation are noncompetitive agonists.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Antagonistic Control of Genetic Circuit Performance for Rapid Analysis of Targeted Enzyme Activity in Living Cells.Frontiers in molecular biosciences · 2020Article
- Allosteric Modulation of Cannabinoid Receptor 1-Current Challenges and Future Opportunities.International journal of molecular sciences · 2019Review
- Tracing Potential Covalent Inhibitors of an E3 Ubiquitin Ligase through Target-Focused Modelling.Molecules (Basel, Switzerland) · 2019Article
- G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence.Computational and structural biotechnology journal · 2019Review
- Exploring the Structural Mechanism of Covalently Bound E3 Ubiquitin Ligase: Catalytic or Allosteric Inhibition?The protein journal · 2018Article
- Involvement of Allosteric Effect and KInternational journal of molecular sciences · 2018Article
- KK-92A, a novel GABAPsychopharmacology · 2017Article
- Population Pharmacokinetics and Pharmacodynamics of the Calcimimetic Etelcalcetide in Chronic Kidney Disease and Secondary Hyperparathyroidism Receiving Hemodialysis.CPT: pharmacometrics & systems pharmacology · 2016Article
- Understanding the role of prostaglandin E2 in regulating human platelet activity in health and disease.Thrombosis research · 2015Review
- Membrane modulates affinity for calcium ion to create an apparent cooperative binding response by annexin a5.Biophysical journal · 2013Article
- Design of peptide and peptidomimetic ligands with novel pharmacological activity profiles.Annual review of pharmacology and toxicology · 2013Review
- In vitro pharmacological characterization of RXFP3 allosterism: an example of probe dependency.PloS one · 2012Article
- Positive allosteric modulators as an approach to nicotinic acetylcholine receptor-targeted therapeutics: advantages and limitations.Biochemical pharmacology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The description of the allosteric modification of receptors to affect changes in their function requires a model that considers the effects of the modulator on both agonist affinity and efficacy. A model is presented which describes changes in affinity in terms of the constant alpha (ratio of affinity in the presence vs the absence of modulator) and also the constant xi (ratio of intrinsic efficacy of the agonist in the presence vs absence of modulator). This allows independent effects of both affinity and efficacy and allows the modeling of any change in the dose-response curve to an agonist after treatment with modulator. Examples are given where this type of model can predict effects of modulators that reduce efficacy but actually increase affinity of agonist (i.e. ifenprodil) and also of modulators that block the action of some agonists (the CXCR4 agonist SDF-1alpha by the antagonist AMD3100) but not others for the same receptor (SDF-1alpha peptide fragments RSVM and ASLW).'All models are wrong...but some are useful...'anonymous environmental scientist.
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.