ArticleThe Journal of biological chemistry2013
A physiologically required G protein-coupled receptor (GPCR)-regulator of G protein signaling (RGS) interaction that compartmentalizes RGS activity.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Exploring GPCR conformational dynamics using single-molecule fluorescence.Methods (San Diego, Calif.) · 2024Review
- Article
- Regulator of G protein signaling 5 restricts neutrophil chemotaxis and trafficking.The Journal of biological chemistry · 2018Article
- The Ancient Link between G-Protein-Coupled Receptors and C-Terminal Phospholipid Kinase Domains.mBio · 2018Article
- Regulator of G protein signaling 4 inhibits human melanoma cells proliferation and invasion through the PI3K/AKT signaling pathway.Oncotarget · 2017Article
- Structural determinants at the M2 muscarinic receptor modulate the RGS4-GIRK response to pilocarpine by impairment of the receptor voltage sensitivity.Scientific reports · 2017Article
- C-terminus of OX2R significantly affects downstream signaling pathways.Molecular medicine reports · 2017Article
- Spatial focalization of pheromone/MAPK signaling triggers commitment to cell-cell fusion.Genes & development · 2016Article
- Modulation of Glucagon Receptor Pharmacology by Receptor Activity-modifying Protein-2 (RAMP2).The Journal of biological chemistry · 2015Article
- RGS4 regulates partial agonism of the M2 muscarinic receptor-activated K+ currents.The Journal of physiology · 2014Article
- TINAGL1 and B3GALNT1 are potential therapy target genes to suppress metastasis in non-small cell lung cancer.BMC genomics · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) can interact with regulator of G protein signaling (RGS) proteins. However, the effects of such interactions on signal transduction and their physiological relevance have been largely undetermined. Ligand-bound GPCRs initiate by promoting exchange of GDP for GTP on the Gα subunit of heterotrimeric G proteins. Signaling is terminated by hydrolysis of GTP to GDP through intrinsic GTPase activity of the Gα subunit, a reaction catalyzed by RGS proteins. Using yeast as a tool to study GPCR signaling in isolation, we define an interaction between the cognate GPCR (Mam2) and RGS (Rgs1), mapping the interaction domains. This reaction tethers Rgs1 at the plasma membrane and is essential for physiological signaling response. In vivo quantitative data inform the development of a kinetic model of the GTPase cycle, which extends previous attempts by including GPCR-RGS interactions. In vivo and in silico data confirm that GPCR-RGS interactions can impose an additional layer of regulation through mediating RGS subcellular localization to compartmentalize RGS activity within a cell, thus highlighting their importance as potential targets to modulate GPCR signaling pathways.
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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.