ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Endogenous regulator of G-protein signaling proteins modify N-type calcium channel modulation in rat sympathetic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. 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, 74 citations in OpenAlex.
- Roles for Regulator of G Protein Signaling Proteins in Synaptic Signaling and Plasticity.Molecular pharmacology · 2016Review
- Control of striatal signaling by g protein regulators.Frontiers in neuroanatomy · 2011Article
- Regulators of G-protein signaling accelerate GPCR signaling kinetics and govern sensitivity solely by accelerating GTPase activity.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Modulation of alpha2-adrenoceptor functions by heterotrimeric Galphai protein isoforms.The Journal of pharmacology and experimental therapeutics · 2009Article
- Pleiotropic phenotype of a genomic knock-in of an RGS-insensitive G184S Gnai2 allele.Molecular and cellular biology · 2006Article
- Regulation of mouse hepatic genes in response to diet induced obesity, insulin resistance and fasting induced weight reduction.Nutrition & metabolism · 2005Article
- Computational modeling reveals how interplay between components of a GTPase-cycle module regulates signal transduction.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- RGS3 mediates a calcium-dependent termination of G protein signaling in sensory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Chick RGS2L demonstrates concentration-dependent selectivity for pertussis toxin-sensitive and -insensitive pathways that inhibit L-type Ca2+ channels.The Journal of physiology · 2003Article
- Agonist unbinding from receptor dictates the nature of deactivation kinetics of G protein-gated K+ channels.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Differential regulation of G protein-gated inwardly rectifying K(+) channel kinetics by distinct domains of RGS8.The Journal of physiology · 2001Article
- RGS2 blocks slow muscarinic inhibition of N-type Ca(2+) channels reconstituted in a human cell line.The Journal of physiology · 2001Article
- Endogenous regulators of G protein signaling proteins regulate presynaptic inhibition at rat hippocampal synapses.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Experiments using heterologous overexpression indicate that regulator of G-protein signaling (RGS) proteins play important roles in Gbetagamma-mediated ion channel modulation. However, the roles subserved by endogenous RGS proteins have not been extensively examined because tools for functionally inhibiting natively expressed RGS proteins are lacking. To address this void, we used a strategy in which Galpha(oA) was rendered insensitive to pertussis toxin (PTX) and RGS proteins by site-directed mutagenesis. Either PTX-insensitive (PTX-i) or both PTX- and RGS-insensitive (PTX/RGS-i) mutants of Galpha(oA) were expressed along with Gbeta(1) and Ggamma(2) subunits in rat sympathetic neurons. After overnight treatment with PTX to suppress natively expressed Galpha subunits, voltage-dependent Ca(2+) current inhibition by norepinephrine (NE) (10 microm) was reconstituted in neurons expressing either PTX-i or PTX/RGS-i Galpha(oA). When compared with neurons expressing PTX-i Galpha(oA), the steady-state concentration-response relationships for NE-induced Ca(2+) current inhibition were shifted to lower concentrations in neurons expressing PTX/RGS-i Galpha(oA). In addition to an increase in agonist potency, the expression of PTX/RGS-i Galpha(oA) dramatically retarded the current recovery after agonist removal. Interestingly, the alteration in current recovery was accompanied by a slowing in the onset of current inhibition. Together, our data suggest that endogenous RGS proteins contribute to membrane-delimited Ca(2+) channel modulation by regulating agonist potency and kinetics of G-protein-mediated signaling in neuronal cells.
Indexed as
Identifiers
10844018PMC6772464W2109449751What 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.