ArticleProceedings of the National Academy of Sciences of the United States of America1997
G alpha(o) is necessary for muscarinic regulation of Ca2+ channels in mouse heart.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 144 citations in OpenAlex.
- CB1R activates the epilepsy-associated protein Go to regulate neurotransmitter release and synaptic plasticity in the cerebellum.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular Dynamic Simulations to Determine Individualized Therapy: Tetrabenazine for the GNAO1 Encephalopathy E246K Variant.Molecular diagnosis & therapy · 2024Article
- Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy.Nature cardiovascular research · 2022Article
- Humanization ofBiomedicines · 2020Article
- Genome-wide association study identifies genes associated with neuropathy in patients with head and neck cancer.Scientific reports · 2018Article
- Article
- Prioritizing the development of mouse models for childhood brain disorders.Neuropharmacology · 2016Review
- Phenotypic spectrum of GNAO1 variants: epileptic encephalopathy to involuntary movements with severe developmental delay.European journal of human genetics : EJHG · 2016Article
- Inhibitory G proteins and their receptors: emerging therapeutic targets for obesity and diabetes.Experimental & molecular medicine · 2014Review
- Gain-of-function mutation in Gnao1: a murine model of epileptiform encephalopathy (EIEE17)?Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- De Novo mutations in GNAO1, encoding a Gαo subunit of heterotrimeric G proteins, cause epileptic encephalopathy.American journal of human genetics · 2013Article
- Go2 G protein mediates galanin inhibitory effects on insulin release from pancreatic β cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The Role of Inhibitory G Proteins and Regulators of G Protein Signaling in the in vivo Control of Heart Rate and Predisposition to Cardiac Arrhythmias.Frontiers in physiology · 2012Article
- μ-Opioid receptor coupling to Gα(o) plays an important role in opioid antinociception.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- PTPBR7 binding proteins in myelinating neurons of the mouse brain.International journal of biological sciences · 2011Article
- Differentiation of human T cells alters their repertoire of G protein alpha-subunits.The Journal of biological chemistry · 2010Article
- Gαo represses insulin secretion by reducing vesicular docking in pancreatic beta-cells.Diabetes · 2010Article
- Genetic disruption of G proteins, G(i2)alpha or G(o)alpha, does not abolish inotropic and chronotropic effects of stimulating muscarinic cholinoceptors in atrium.British journal of pharmacology · 2009Article
- Drosophila GoLoco-protein Pins is a target of Galpha(o)-mediated G protein-coupled receptor signaling.Molecular biology of the cell · 2009Article
- Molecular mechanisms of go signaling.Neuro-Signals · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Heterotrimeric G proteins, composed of G alpha and G betagamma subunits, transmit signals from cell surface receptors to cellular effector enzymes and ion channels. The G alpha(o) protein is the most abundant G alpha subtype in the nervous system, but it is also found in the heart. Its function is not completely known, although it is required for regulation of N-type Ca2+ channels in GH3 cells and also interacts with GAP43, a major protein in growth cones, suggesting a role in neuronal pathfinding. To analyze the function of G alpha(o), we have generated mice lacking both isoforms of G alpha(o) by homologous recombination. Surprisingly, the nervous system is grossly intact, despite the fact that G alpha(o) makes up 0.2-0.5% of brain particulate protein and 10% of the growth cone membrane. The G alpha(o)-/- mice do suffer tremors and occasional seizures, but there is no obvious histologic abnormality in the nervous system. In contrast, G alpha(o)-/- mice have a clear and specific defect in ion channel regulation in the heart. Normal muscarinic regulation of L-type calcium channels in ventricular myocytes is absent in the mutant mice. The L-type calcium channel responds normally to isoproterenol, but there is no evident muscarinic inhibition. Muscarinic regulation of atrial K+ channels is normal, as is the electrocardiogram. The levels of other G alpha subunits (G alpha(s), G alpha(q), and G alpha(i)) are unchanged in the hearts of G alpha(o)-/- mice, but the amount of G betagamma is decreased. Whichever subunit, G alpha(o) or G betagamma, carries the signal forward, these studies show that muscarinic inhibition of L-type Ca2+ channels requires coupling of the muscarinic receptor to G alpha(o). Other cardiac G alpha subunits cannot substitute.
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.