ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Regulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GTPase-activating proteins.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- A Meta-Analysis of Brain DNA Methylation Across Sex, Age, and Alzheimer's Disease Points for Accelerated Epigenetic Aging in Neurodegeneration.Frontiers in aging neuroscience · 2021Pooled it
- Brain-targeted epigenetic effects of two emerging psychoplastogens: ketamine & MDMA.Translational psychiatry · 2026Article
- Rac1 Constrains Memory Consolidation.eNeuro · 2026Article
- Association of maternal smoking during pregnancy with youth depression and subsequent adult chronic diseases in offspring.Translational psychiatry · 2026Article
- Plasma circulating extracellular vesicles reveal dysregulation of synaptic signaling in SHIV-infected rhesus macaque.Cell communication and signaling : CCS · 2025Article
- Hippocampal dipeptidyl peptidase 9 bidirectionally regulates memory associated with synaptic plasticity.Journal of advanced research · 2025Article
- Article
- Presynaptic Rac1 in the hippocampus selectively regulates working memory.bioRxiv : the preprint server for biology · 2024Article
- Review
- The Evaluation of Rac1 Signaling as a Potential Therapeutic Target of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Roles of Rac1-Dependent Intrinsic Forgetting in Memory-Related Brain Disorders: Demon or Angel.International journal of molecular sciences · 2023Review
- S-Ketamine Exerts Antidepressant Effects by Regulating Rac1 GTPase Mediated Synaptic Plasticity in the Hippocampus of Stressed Rats.Cellular and molecular neurobiology · 2023Article
- Rac-maninoff and Rho-vel: The symphony of Rho-GTPase signaling at excitatory synapses.Small GTPases · 2022Article
- Inhibition of Rac1 in ventral hippocampal excitatory neurons improves social recognition memory and synaptic plasticity.Frontiers in aging neuroscience · 2022Article
- Characterization of novel CTNNB1 mutation in Craniopharyngioma by whole-genome sequencing.Molecular cancer · 2021Article
- Review
- Novel Alzheimer's disease risk variants identified based on whole-genome sequencing of APOE ε4 carriers.Translational psychiatry · 2021Article
- The Rac-GEF Tiam1 Promotes Dendrite and Synapse Stabilization of Dentate Granule Cells and Restricts Hippocampal-Dependent Memory Functions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Rho Signaling in Synaptic Plasticity, Memory, and Brain Disorders.Frontiers in cell and developmental biology · 2021Review
- Pharmacological Modulators of Small GTPases of Rho Family in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 3 countries.
Funding
Abstract
Rho family small GTPases are important regulators of neuronal development. Defective Rho regulation causes nervous system dysfunctions including mental retardation and Alzheimer's disease. Rac1, a member of the Rho family, regulates dendritic spines and excitatory synapses, but relatively little is known about how synaptic Rac1 is negatively regulated. Breakpoint cluster region (BCR) is a Rac GTPase-activating protein known to form a fusion protein with the c-Abl tyrosine kinase in Philadelphia chromosome-positive chronic myelogenous leukemia. Despite the fact that BCR mRNAs are abundantly expressed in the brain, the neural functions of BCR protein have remained obscure. We report here that BCR and its close relative active BCR-related (ABR) localize at excitatory synapses and directly interact with PSD-95, an abundant postsynaptic scaffolding protein. Mice deficient for BCR or ABR show enhanced basal Rac1 activity but only a small increase in spine density. Importantly, mice lacking BCR or ABR exhibit a marked decrease in the maintenance, but not induction, of long-term potentiation, and show impaired spatial and object recognition memory. These results suggest that BCR and ABR have novel roles in the regulation of synaptic Rac1 signaling, synaptic plasticity, and learning and memory, and that excessive Rac1 activity negatively affects synaptic and cognitive functions.
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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.