ArticleThe Journal of biological chemistry2013
Modulation of GluK2a subunit-containing kainate receptors by 14-3-3 proteins.
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. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- 14-3-3 Dysfunction in Dorsal Hippocampus CA1 (dCA1) Induces Psychomotor BehaviorFrontiers in molecular neuroscience · 2022Article
- 14-3-3 proteins promote synaptic localization of N-methyl d-aspartate receptors (NMDARs) in mouse hippocampal and cortical neurons.PloS one · 2021Article
- SUMOylation of synaptic and synapse-associated proteins: An update.Journal of neurochemistry · 2021Review
- Olig2 SUMOylation protects against genotoxic damage response by antagonizing p53 gene targeting.Cell death and differentiation · 2020Article
- 14-3-3 Proteins in Glutamatergic Synapses.Neural plasticity · 2018Review
- PKC SUMOylation inhibits the binding of 14-3-3τ to GluK2.Channels (Austin, Tex.) · 2017Article
- 14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.The Journal of biological chemistry · 2015Article
- Trafficking of kainate receptors.Membranes · 2014Review
- Depletion of 14-3-3γ reduces the surface expression of Transient Receptor Potential Melastatin 4b (TRPM4b) channels and attenuates TRPM4b-mediated glutamate-induced neuronal cell death.Molecular brain · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kainate receptors (KARs) are one of the ionotropic glutamate receptors that mediate excitatory postsynaptic currents (EPSCs) with characteristically slow kinetics. Although mechanisms for the slow kinetics of KAR-EPSCs are not totally understood, recent evidence has implicated a regulatory role of KAR-associated proteins. Here, we report that decay kinetics of GluK2a-containing receptors is modulated by closely associated 14-3-3 proteins. 14-3-3 binding requires PKC-dependent phosphorylation of serine residues localized in the carboxyl tail of the GluK2a subunit. In transfected cells, 14-3-3 binding to GluK2a slows desensitization kinetics of both homomeric GluK2a and heteromeric GluK2a/GluK5 receptors. Moreover, KAR-EPSCs at mossy fiber-CA3 synapses decay significantly faster in the 14-3-3 functional knock-out mice. Collectively, these results demonstrate that 14-3-3 proteins are an important regulator of GluK2a-containing KARs and may contribute to the slow decay kinetics of native KAR-EPSCs.
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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.