ArticleProceedings of the National Academy of Sciences of the United States of America2016
Kalirin and Trio proteins serve critical roles in excitatory synaptic transmission and LTP.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 100 citations in OpenAlex.
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Genetic Variants from Large Cohorts and Familial Studies Implicate Common Mechanisms in Schizophrenia.Biology · 2026Review
- Early-life gut microbiome maturity regulates blood-brain barrier and cognitive development.Gut microbes · 2025Article
- Trio and CRMP2 regulate axon branching and Semaphorin3A signaling.Communications biology · 2025Article
- Rho signaling promotes cell excitability and synaptic transmission.bioRxiv : the preprint server for biology · 2025Article
- Comprehensive profiling of transcription factors for reprogramming human astrocytes to neuronal cells through endogenous CRISPR-based gene activation.bioRxiv : the preprint server for biology · 2025Article
- Lithium normalizes ASD-related neuronal, synaptic, and behavioral phenotypes in DYRK1A-knockin mice.Molecular psychiatry · 2025Article
- Both GEF domains of the autism and developmental epileptic encephalopathy-associated Trio protein are required for proper tangential migration of GABAergic interneurons.Molecular psychiatry · 2025Article
- Dentate Gyrus Morphogenesis is Regulated by an Autism Risk Gene Trio Function in Granule Cells.Neuroscience bulletin · 2025Article
- Human stem cell-based models to study synaptic dysfunction and cognition in schizophrenia: A narrative review.Schizophrenia research · 2024Review
- A Novel Single-Color FRET Sensor for Rho-Kinase Reveals Calcium-Dependent Activation of RhoA and ROCK.Sensors (Basel, Switzerland) · 2024Article
- RhoGEF Tiam2 Regulates Glutamatergic Synaptic Transmission in Hippocampal CA1 Pyramidal Neurons.eNeuro · 2024Article
- Detection of autism spectrum disorder-related pathogenic trio variants by a novel structure-based approach.Molecular autism · 2024Article
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.bioRxiv : the preprint server for biology · 2024Article
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.PloS one · 2024Article
- Protein 4.1N Plays a Cell Type-Specific Role in Hippocampal Glutamatergic Synapse Regulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Regulation of NLGN3 and the Synaptic Rho-GEF Signaling Pathway by CDK5.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Early developmental deletion of forebrain Ank2 causes seizure-related phenotypes by reshaping the synaptic proteome.Cell reports · 2023Article
- Interneuron odyssey: molecular mechanisms of tangential migration.Frontiers in neural circuits · 2023Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanism underlying long-term potentiation (LTP) is critical for understanding learning and memory. CaMKII, a key kinase involved in LTP, is both necessary and sufficient for LTP induction. However, how CaMKII gives rise to LTP is currently unknown. Recent studies suggest that Rho GTPases are necessary for LTP. Rho GTPases are activated by Rho guanine exchange factors (RhoGEFs), but the RhoGEF(s) required for LTP also remain unknown. Here, using a combination of molecular, electrophysiological, and imaging techniques, we show that the RhoGEF Kalirin and its paralog Trio play critical and redundant roles in excitatory synapse structure and function. Furthermore, we show that CaMKII phosphorylation of Kalirin is sufficient to enhance synaptic AMPA receptor expression, and that preventing CaMKII signaling through Kalirin and Trio prevents LTP induction. Thus, our data identify Kalirin and Trio as the elusive targets of CaMKII phosphorylation responsible for AMPA receptor up-regulation during LTP.
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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.