ArticleNeuro-Signals2010
Association of the small GTPase Rheb with the NMDA receptor subunit NR3A.
Article in Neuro-Signals, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Emerging roles of GluN3-containing NMDA receptors in the CNS.Nature reviews. Neuroscience · 2016Review
- Antidepressant action of ketamine via mTOR is mediated by inhibition of nitrergic Rheb degradation.Molecular psychiatry · 2016Article
- Neonatal seizures alter NMDA glutamate receptor GluN2A and 3A subunit expression and function in hippocampal CA1 neurons.Frontiers in cellular neuroscience · 2015Article
- Direct Interaction between Ras Homolog Enriched in Brain and FK506 Binding Protein 38 in Cashmere Goat Fetal Fibroblast Cells.Asian-Australasian journal of animal sciences · 2014Article
- GluN3A promotes dendritic spine pruning and destabilization during postnatal development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- GluN3A: an NMDA receptor subunit with exquisite properties and functions.Neural plasticity · 2013Review
- Mechanisms of specificity in neuronal activity-regulated gene transcription.Progress in neurobiology · 2011Review
- Frontier of epilepsy research - mTOR signaling pathway.Experimental & molecular medicine · 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
8 authors at 4 institutions in 3 countries.
Funding
Abstract
The NMDAR subunit NR3A is most highly expressed during the second postnatal week, when synaptogenesis reaches peak levels. Genetic ablation or overexpression of the NR3A subunit negatively interferes with the maturation of cortical synapses and leads to changes in the shape and number of dendritic spines, the density of which is increased in NR3A knock-out mice and decreased in NR3A-overexpressing transgenic mice. Alterations in spine density have been linked to dysregulation of mTOR signaling and synaptic protein translation. Using a yeast two-hybrid system, we identified the mTOR-activating GTPase Rheb as an interacting protein of the NMDAR subunit NR3A. We confirmed the interaction in mammalian cells by expressing recombinant Rheb and NR3A and showed that Rheb and NR3A could be co-immunoprecipitated from synaptic plasma membranes from the developing rat brain. These data suggest that NR3A sequesters synaptic Rheb and might thus function as a break of the mTOR-dependent synaptic translation of protein.
Indexed as
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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.