ArticleJournal of cell science2018
ADAR2-mediated Q/R editing of GluK2 regulates kainate receptor upscaling in response to suppression of synaptic activity.
Article in Journal of cell science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Evolution of Engineered ADAR-Based RNA Editing Systems.International journal of molecular sciences · 2026Review
- ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity.Science signaling · 2025Article
- Comprehensive characterization of the transcriptional landscape in Alzheimer's disease (AD) brains.Science advances · 2025Article
- Two Signaling Modes Are Better than One: Flux-Independent Signaling by Ionotropic Glutamate Receptors Is Coming of Age.Biomedicines · 2024Review
- Calcium-permeable AMPA and kainate receptors of GABAergic neurons.Biophysical reviews · 2024Review
- Aberrant glycosylation in schizophrenia: insights into pathophysiological mechanisms and therapeutic potentials.Frontiers in pharmacology · 2024Review
- GluK2 Q/R editing regulates kainate receptor signaling and long-term potentiation of AMPA receptors.iScience · 2023Article
- Reduction of A-to-I RNA editing in the failing human heart regulates formation of circular RNAs.Basic research in cardiology · 2022Article
- Structure, Function, and Regulation of the Kainate Receptor.Sub-cellular biochemistry · 2022Review
- Sustained postsynaptic kainate receptor activation downregulates AMPA receptor surface expression and induces hippocampal LTD.iScience · 2021Article
- Neurotrophic effects of Botulinum neurotoxin type A in hippocampal neurons involve activation of Rac1 by the non-catalytic heavy chain (HCIBRO neuroscience reports · 2021Article
- Spatiotemporal Regulation of Transcript Isoform Expression in the Hippocampus.Frontiers in molecular neuroscience · 2021Article
- Guanosine modulates SUMO2/3-ylation in neurons and astrocytes via adenosine receptors.Purinergic signalling · 2020Article
- Membrane and synaptic defects leading to neurodegeneration in Adar mutant Drosophila are rescued by increased autophagy.BMC biology · 2020Article
- Review
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Kainate receptors (KARs) regulate neuronal excitability and network function. Most KARs contain the subunit GluK2 (also known as GRIK2), and the properties of these receptors are determined in part by ADAR2 (also known as ADARB1)-mediated mRNA editing of GluK2, which changes a genomically encoded glutamine residue into an arginine residue (Q/R editing). Suppression of synaptic activity reduces ADAR2-dependent Q/R editing of GluK2 with a consequential increase in GluK2-containing KAR surface expression. However, the mechanism underlying this reduction in GluK2 editing has not been addressed. Here, we show that induction of KAR upscaling, a phenomenon in which surface expression of receptors is increased in response to a chronic decrease in synaptic activity, results in proteasomal degradation of ADAR2, which reduces GluK2 Q/R editing. Because KARs incorporating unedited GluK2(Q) assemble and exit the ER more efficiently, this leads to an upscaling of KAR surface expression. Consistent with this, we demonstrate that partial ADAR2 knockdown phenocopies and occludes KAR upscaling. Moreover, we show that although the AMPA receptor (AMPAR) subunit GluA2 (also known as GRIA2) also undergoes ADAR2-dependent Q/R editing, this process does not mediate AMPAR upscaling. These data demonstrate that activity-dependent regulation of ADAR2 proteostasis and GluK2 Q/R editing are key determinants of KAR, but not AMPAR, trafficking and upscaling.This article has an associated First Person interview with the first author of the paper.
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