Reciprocal signaling between translational control pathways and synaptic proteins in autism spectrum disorders.
about
LTD-like molecular pathways in developmental synaptic pruningAutism As a Disorder of High IntelligenceMaternal immune activation: Implications for neuropsychiatric disorders.Fragile X mental retardation protein: from autism to neurodegenerative disease.Tuberous Sclerosis: A New Frontier in Targeted Treatment of AutismeIF4E/Fmr1 double mutant mice display cognitive impairment in addition to ASD-like behaviors.Current Perspectives in Autism Spectrum Disorder: From Genes to Therapy.The use of stem cells to study autism spectrum disorderMaternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder.Immune mediators in the brain and peripheral tissues in autism spectrum disorder.Genetic Animal Models for Autism Spectrum Disorder.Unifying Views of Autism Spectrum Disorders: A Consideration of Autoregulatory Feedback Loops.Lessons learned from studying syndromic autism spectrum disorders.Spatially and temporally regulating translation via mRNA-binding proteins in cellular and neuronal function.Translation is actively regulated during the differentiation of CD8+ effector T cells.Hierarchical cortical transcriptome disorganization in autism.Increased signaling by the autism-related Engrailed-2 protein enhances dendritic branching and spine density, alters synaptic structural matching, and exaggerates protein synthesis.Autism and Epilepsy: Exploring the Relationship Using Experimental Models.Activation of a novel p70 S6 kinase 1-dependent intracellular cascade in the basolateral nucleus of the amygdala is required for the acquisition of extinction memory.Common functional variants of the glutamatergic system in Autism spectrum disorder with high and low intellectual abilities.Reducing eIF4E-eIF4G interactions restores the balance between protein synthesis and actin dynamics in fragile X syndrome model mice.Foxp1 in Forebrain Pyramidal Neurons Controls Gene Expression Required for Spatial Learning and Synaptic Plasticity.Cerebrolysin prevents deficits in social behavior, repetitive conduct, and synaptic inhibition in a rat model of autism.Aberrant cognitive phenotypes and altered hippocampal BDNF expression related to epigenetic modifications in mice lacking the post-synaptic scaffolding protein SHANK1: Implications for autism spectrum disorder.Excessive UBE3A dosage impairs retinoic acid signaling and synaptic plasticity in autism spectrum disorders.Rescue of learning and memory deficits in the human non-syndromic intellectual disability cereblon knockout mouse model by targeting the AMPK-mTORC1 translational pathway.mTOR signaling in VIP neurons regulates circadian clock synchrony and olfaction.
P2860
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P2860
Reciprocal signaling between translational control pathways and synaptic proteins in autism spectrum disorders.
description
2014 nî lūn-bûn
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2014年の論文
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2014年学术文章
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2014年学术文章
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2014年学术文章
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2014年学术文章
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2014年學術文章
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name
Reciprocal signaling between t ...... in autism spectrum disorders.
@en
type
label
Reciprocal signaling between t ...... in autism spectrum disorders.
@en
prefLabel
Reciprocal signaling between t ...... in autism spectrum disorders.
@en
P2860
P1433
P1476
Reciprocal signaling between t ...... in autism spectrum disorders.
@en
P2093
Emanuela Santini
Eric Klann
P2860
P356
10.1126/SCISIGNAL.2005832
P577
2014-10-28T00:00:00Z