{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Araki Y"],"funding":["NIMH NIH HHS","NINDS NIH HHS"],"pagination":["eadk1291"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11188940"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["383(6686)"],"pubmed_abstract":["SynGAP is an abundant synaptic GTPase-activating protein (GAP) critical for synaptic plasticity, learning, memory, and cognition. Mutations in <i>SYNGAP1</i> in humans result in intellectual disability, autistic-like behaviors, and epilepsy. Heterozygous <i>Syngap1</i>-knockout mice display deficits in synaptic plasticity, learning, and memory and exhibit seizures. It is unclear whether SynGAP imparts structural properties at synapses independently of its GAP activity. Here, we report that inactivating mutations within the GAP domain do not inhibit synaptic plasticity or cause behavioral deficits. Instead, SynGAP modulates synaptic strength by physically competing with the AMPA-receptor-TARP excitatory receptor complex in the formation of molecular condensates with synaptic scaffolding pro"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["SynGAP regulates synaptic plasticity and cognition independently of its catalytic activity."],"pmcid":["PMC11188940"],"funding_grant_id":["T32 NS091018","R01 MH112151","T32 MH015330","R01 NS036715"],"pubmed_authors":["Rajkovich KE","Johnson RC","Araki Y","Kirkwood A","Huganir R","Gerber EE","Hong I","Tran THN","Liu B","Gamache TR","Zhu Q"],"additional_accession":[]},"is_claimable":false,"name":"SynGAP regulates synaptic plasticity and cognition independently of its catalytic activity.","description":"SynGAP is an abundant synaptic GTPase-activating protein (GAP) critical for synaptic plasticity, learning, memory, and cognition. Mutations in <i>SYNGAP1</i> in humans result in intellectual disability, autistic-like behaviors, and epilepsy. Heterozygous <i>Syngap1</i>-knockout mice display deficits in synaptic plasticity, learning, and memory and exhibit seizures. It is unclear whether SynGAP imparts structural properties at synapses independently of its GAP activity. Here, we report that inactivating mutations within the GAP domain do not inhibit synaptic plasticity or cause behavioral deficits. Instead, SynGAP modulates synaptic strength by physically competing with the AMPA-receptor-TARP excitatory receptor complex in the formation of molecular condensates with synaptic scaffolding pro","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-04T02:45:36.979Z","creation":"2025-04-04T02:45:36.979Z"},"accession":"S-EPMC11188940","cross_references":{"pubmed":["38422154"],"doi":["10.1126/science.adk1291"]}}