ArticleJournal of neurochemistry2020
SynGAP splice variants display heterogeneous spatio-temporal expression and subcellular distribution in the developing mammalian brain.
Article in Journal of neurochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Technologies to measure and modulate protein subcellular localization.Nature reviews. Molecular cell biology · 2026Review
- The Synaptic Clock: SynGAP1 as a Molecular Timer of Postsynaptic Density Consolidation.Biomolecules · 2026Review
- Missense mutations on SynGAP C2 domain impair membrane diffusion.Protein science : a publication of the Protein Society · 2026Article
- Syngap1 Synchronizes Relative Neuronal Maturation Across Cortical Areas to Organize Distributed Functional Networks.bioRxiv : the preprint server for biology · 2026Article
- Syngap1 and the development of murine neocortical progenitor cells.Nature communications · 2025Article
- The Endo-GeneScreen platform identifies drug-like probes that regulate endogenous protein levels within physiological contexts.Nature communications · 2025Article
- CRISPR-mediated transcriptional activation as a mutation-independent therapeutic strategy forbioRxiv : the preprint server for biology · 2025Article
- Article
- Dizocilpine Does Not AlterInternational journal of molecular sciences · 2025Article
- Dissociation of SYNGAP1 enzymatic and structural roles: Intrinsic excitability and seizure susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dissociation of SYNGAP1 Enzymatic and Structural Roles: Intrinsic Excitability and Seizure Susceptibility.bioRxiv : the preprint server for biology · 2025Article
- DevelopmentalThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Haploinsufficiency ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.Translational psychiatry · 2024Article
- Hyperexcitability and translational phenotypes in a preclinical mouse model ofResearch square · 2024Article
- Context-dependent hyperactivity inFrontiers in molecular neuroscience · 2024Article
- Developmental outcome of electroencephalographic findings inFrontiers in cell and developmental biology · 2024Article
- RNA-based translation activators for targeted gene upregulation.Nature communications · 2023Article
- Mouse models ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mouse models ofbioRxiv : the preprint server for biology · 2023Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
The SynGAP protein is a major regulator of synapse biology and neural circuit function. Genetic variants linked to epilepsy and intellectual disability disrupt synaptic function and neural excitability. SynGAP has been involved in multiple signaling pathways and can regulate small GTPases with very different roles. Yet, the molecular bases behind this pleiotropy are poorly understood. We hypothesize that different SynGAP isoforms will mediate different sets of functions and that deciphering their spatio-temporal expression and subcellular localization will accelerate understanding their multiple functions. Using isoform-specific antibodies recognizing SynGAP in mouse and human samples we found distinctive developmental expression patterns for all SynGAP isoforms in five mouse brain areas. Particularly noticeable was the delayed expression of SynGAP-α1 isoforms, which directly bind to postsynaptic density-95, in cortex and hippocampus during the first 2 weeks of postnatal development. Suggesting that during this period other isoforms would have a more prominent role. Furthermore, we observed subcellular localization differences between isoforms, particularly throughout postnatal development. Consistent with previous reports, SynGAP was enriched in the postsynaptic density in the mature forebrain. However, SynGAP was predominantly found in non-synaptic locations in a period of early postnatal development highly sensitive to SynGAP levels. While, α1 isoforms were always found enriched in the postsynaptic density, α2 isoforms changed from a non-synaptic to a mostly postsynaptic density localization with age and β isoforms were always found enriched in non-synaptic locations. The differential expression and subcellular distribution of SynGAP isoforms may contribute to isoform-specific regulation of small GTPases, explaining SynGAP pleiotropy.
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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.