ArticleNature communications2022
Kinetic model of GPCR-G protein interactions reveals allokairic modulation of signaling.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- SSTR2 receptor states and cellular metabolism modulateEANM innovation · 2026Article
- Mapping the Binding Landscape of Allosteric Inhibitor G6PDi-1 on Human G6PD.The journal of physical chemistry letters · 2026Article
- Kinetic model of partial agonism reveals cellular basis of ligand efficacy.The Journal of biological chemistry · 2026Article
- Article
- Chemical multiplexing in the nervous system: molecular architecture, functional stratification, and pathophysiological plasticity of neuropeptide-classical neurotransmitter cotransmission.Frontiers in molecular neuroscience · 2026Review
- Structural determinants of G protein subtype selectivity at the serotonin receptor 5-HT1A.Science advances · 2025Article
- Hidden GPCR structural transitions addressed by multiple walker supervised molecular dynamics (mwSuMD).eLife · 2025Article
- Exploiting Cell-Based Assays to Accelerate Drug Development for G Protein-Coupled Receptors.International journal of molecular sciences · 2024Review
- Article
- Ligand-Free Signaling of G-Protein-Coupled Receptors: Physiology, Pharmacology, and Genetics.Molecules (Basel, Switzerland) · 2023Review
- Advancements in G protein-coupled receptor biosensors to study GPCR-G protein coupling.British journal of pharmacology · 2023Review
- Elucidation of a dynamic interplay between a beta-2 adrenergic receptor, its agonist, and stimulatory G protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gq Signaling in Autophagy Control: Between Chemical and Mechanical Cues.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Established models of ternary complex formation between hormone, G protein coupled receptor (GPCR), and G protein assume that all interactions occur under equilibrium conditions. However, recent studies have established that the lifetimes of these interactions are comparable to the duration of hormone activated GPCR signaling. To simulate interactions during such non-equilibrium conditions, we propose a kinetic model wherein the receptor undergoes rate-limiting transitions between two hormone-bound active states. Simulations, using experimentally measured parameters, demonstrate transient states in ternary complex formation, and delineate the phenomenon of GPCR priming, wherein non-cognate G proteins substantially enhance cognate G protein signaling. Our model reveals that kinetic barriers of slow receptor interconversion can be overcome through allokairic modulation, a regulatory mechanism of ternary complex formation and downstream signaling.
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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.