ArticleNature communications2012
SynGAP isoforms exert opposing effects on synaptic strength.
Article in Nature communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 96 citations in OpenAlex.
- The Synaptic Clock: SynGAP1 as a Molecular Timer of Postsynaptic Density Consolidation.Biomolecules · 2026Review
- HDAC Inhibition Reshapes Splicing of Synaptic Plasticity-Related Genes and Neural Network Dynamics.Cellular and molecular neurobiology · 2026Article
- Loss of Necdin causes social deficit and aberrant synaptic function through destabilization of SynGAP.Molecular psychiatry · 2026Article
- AAV delivery of full-length SYNGAP1 rescues epileptic and behavioral phenotypes in a mouse model of SYNGAP1-related disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- CRISPR-mediated transcriptional activation as a mutation-independent therapeutic strategy forbioRxiv : the preprint server for biology · 2025Article
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- Convergent depression of activity-dependent bulk endocytosis in rodent models of autism spectrum disorder.Molecular autism · 2025Article
- Integrated multi-omic characterizations of the synapse reveal RNA processing factors and ubiquitin ligases associated with neurodevelopmental disorders.Cell systems · 2025Article
- Reply to "Concerns regarding the interpretation of Shank3 protein isoforms expressed in Shank3BMolecular psychiatry · 2025Article
- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- 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
- Context-dependent hyperactivity inFrontiers in molecular neuroscience · 2024Article
- Understanding the role of AMPA receptors in autism: insights from circuit and synapse dysfunction.Frontiers in psychiatry · 2024Review
- Mouse models ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Liquid-liquid phase separation in synaptopathies.Neuroprotection (Chichester, England) · 2023Review
- Mouse models ofbioRxiv : the preprint server for biology · 2023Article
- Article
- The ALS-Related SynGAP1 Pathogenic Variant Causes Dendritic Spine Loss: Potential Mechanisms of Early-Stage ALS Progression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative promoter usage and alternative splicing enable diversification of the transcriptome. Here we demonstrate that the function of Synaptic GTPase-Activating Protein (SynGAP), a key synaptic protein, is determined by the combination of its amino-terminal sequence with its carboxy-terminal sequence. 5' rapid amplification of cDNA ends and primer extension show that different N-terminal protein sequences arise through alternative promoter usage that are regulated by synaptic activity and postnatal age. Heterogeneity in C-terminal protein sequence arises through alternative splicing. Overexpression of SynGAP α1 versus α2 C-termini-containing proteins in hippocampal neurons has opposing effects on synaptic strength, decreasing and increasing miniature excitatory synaptic currents amplitude/frequency, respectively. The magnitude of this C-terminal-dependent effect is modulated by the N-terminal peptide sequence. This is the first demonstration that activity-dependent alternative promoter usage can change the function of a synaptic protein at excitatory synapses. Furthermore, the direction and degree of synaptic modulation exerted by different protein isoforms from a single gene locus is dependent on the combination of differential promoter usage and alternative splicing.
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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.