Pathogenic SYNGAP1 mutations impair cognitive development by disrupting maturation of dendritic spine synapses.
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Neuropathological Mechanisms of Seizures in Autism Spectrum DisorderControl of Dendritic Spine Morphological and Functional Plasticity by Small GTPasesSYNGAP1: Mind the GapModeling psychiatric disorders for developing effective treatmentsOn the Teneurin track: a new synaptic organization molecule emergesTwo knockdown models of the autism genes SYNGAP1 and SHANK3 in zebrafish produce similar behavioral phenotypes associated with embryonic disruptions of brain morphogenesis.Rapid dispersion of SynGAP from synaptic spines triggers AMPA receptor insertion and spine enlargement during LTP.Large-scale neural circuit mapping data analysis accelerated with the graphical processing unit (GPU)Spine pruning drives antipsychotic-sensitive locomotion via circuit control of striatal dopamine.Phase Transition in Postsynaptic Densities Underlies Formation of Synaptic Complexes and Synaptic PlasticityA Subset of Autism-Associated Genes Regulate the Structural Stability of Neurons.Human variants in the neuronal basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) transcription factor complex NPAS4/ARNT2 disrupt functionMET receptor tyrosine kinase controls dendritic complexity, spine morphogenesis, and glutamatergic synapse maturation in the hippocampusAdult restoration of Shank3 expression rescues selective autistic-like phenotypesPrenatal deletion of the RNA-binding protein HuD disrupts postnatal cortical circuit maturation and behaviorSingle nucleotide polymorphism in the neuroplastin locus associates with cortical thickness and intellectual ability in adolescentsSHANK proteins: roles at the synapse and in autism spectrum disorder.Prioritizing the development of mouse models for childhood brain disordersInvestigating mechanisms underlying neurodevelopmental phenotypes of autistic and intellectual disability disorders: a perspective.Reduced cognition in Syngap1 mutants is caused by isolated damage within developing forebrain excitatory neuronsDecrease of SYNGAP1 in GABAergic cells impairs inhibitory synapse connectivity, synaptic inhibition and cognitive function.Epilepsy and Autism.Common DNA methylation alterations in multiple brain regions in autism.Intellectual disability and autism spectrum disorders: causal genes and molecular mechanisms.Structural plasticity: mechanisms and contribution to developmental psychiatric disordersCamkii-mediated phosphorylation regulates distributions of Syngap-α1 and -α2 at the postsynaptic density.Syngap1 haploinsufficiency damages a postnatal critical period of pyramidal cell structural maturation linked to cortical circuit assemblySynGAP regulates protein synthesis and homeostatic synaptic plasticity in developing cortical networks.Phosphorylation of synaptic GTPase-activating protein (synGAP) by Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cyclin-dependent kinase 5 (CDK5) alters the ratio of its GAP activity toward Ras and Rap GTPasesIn-depth protein profiling of the postsynaptic density from mouse hippocampus using data-independent acquisition proteomics.δ-Catenin Regulates Spine Architecture via Cadherin and PDZ-dependent Interactions.Ube3a reinstatement identifies distinct developmental windows in a murine Angelman syndrome model.Input-specific regulation of hippocampal circuit maturation by non-muscle myosin IIB.Altered Expression of ARP2/3 Complex Signaling Pathway Genes in Prefrontal Layer 3 Pyramidal Cells in Schizophrenia.Convergence of Hippocampal Pathophysiology in Syngap+/- and Fmr1-/y Mice.Genetic Demonstration of a Role for Stathmin in Adult Hippocampal Neurogenesis, Spinogenesis, and NMDA Receptor-Dependent Memory.TRIO loss of function is associated with mild intellectual disability and affects dendritic branching and synapse function.In vivo quantitative proteomics of somatosensory cortical synapses shows which protein levels are modulated by sensory deprivationSYNGAP1 links the maturation rate of excitatory synapses to the duration of critical-period synaptic plasticity.The autism-associated MET receptor tyrosine kinase engages early neuronal growth mechanism and controls glutamatergic circuits development in the forebrain
P2860
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P2860
Pathogenic SYNGAP1 mutations impair cognitive development by disrupting maturation of dendritic spine synapses.
description
2012 nî lūn-bûn
@nan
2012 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Pathogenic SYNGAP1 mutations i ...... on of dendritic spine synapses
@nl
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@ast
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@en
type
label
Pathogenic SYNGAP1 mutations i ...... on of dendritic spine synapses
@nl
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@ast
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@en
prefLabel
Pathogenic SYNGAP1 mutations i ...... on of dendritic spine synapses
@nl
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@ast
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@en
P2093
P2860
P50
P3181
P1433
P1476
Pathogenic SYNGAP1 mutations i ...... n of dendritic spine synapses.
@en
P2093
Brian J Wiltgen
Brooke H Miller
Emin D Ozkan
Gavin Rumbaugh
James P Clement
Nicholas J Reish
Thomas K Creson
Xiangmin Xu
P2860
P304
P3181
P356
10.1016/J.CELL.2012.08.045
P407
P577
2012-11-01T00:00:00Z