Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits. - sprookjes - yvandenbroek - TriplyDB

Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits.

Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits.

http://www.wikidata.org/entity/Q29618411

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Whole-exome sequencing supports genetic heterogeneity in childhood apraxia of speech.Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Autism-associated neuroligin-3 mutations commonly impair striatal circuits to boost repetitive behaviors.Candidate autism gene screen identifies critical role for cell-adhesion molecule CASPR2 in dendritic arborization and spine development Neuropathological Mechanisms of Seizures in Autism Spectrum Disorder Clinical and Neurobiological Relevance of Current Animal Models of Autism Spectrum Disorders.Mouse Genetic Models of Human Brain Disorders Cell migration in the developing rodent olfactory system Functional Evaluations of Genes Disrupted in Patients with Tourette's Disorder.Striatal Circuits as a Common Node for Autism Pathophysiology Autism Spectrum Disorders and Drug Addiction: Common Pathways, Common Molecules, Distinct Disorders?New Therapeutic Options for Autism Spectrum Disorder: Experimental Evidences Genetics of Autism Spectrum Disorder: Current Status and Possible Clinical Applications Cellullar insights into cerebral cortical development: focusing on the locomotion mode of neuronal migration Behavioral phenotypes of genetic mouse models of autism.Modeling psychiatric disorders for developing effective treatments Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders Neuronal and microglial regulators of cortical wiring: usual and novel guideposts Converging levels of analysis on a genomic hotspot for psychosis: insights from 22q11.2 deletion syndrome Clinical and experimental studies of potentially pathogenic brain-directed autoantibodies: current knowledge and future directions Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders Following the genes: a framework for animal modeling of psychiatric disorders Genetics in non-genetic model systems Molecular underpinnings of prefrontal cortex development in rodents provide insights into the etiology of neurodevelopmental disorders The molecular basis of cognitive deficits in pervasive developmental disorders Extracellular and Intracellular Signaling for Neuronal Polarity The promise of multi-omics and clinical data integration to identify and target personalized healthcare approaches in autism spectrum disorders Sharing heterogeneous data: the national database for autism research CNVs: harbingers of a rare variant revolution in psychiatric genetics Behavioral and Neuroanatomical Phenotypes in Mouse Models of Autism Axon initial segments: diverse and dynamic neuronal compartments Early hyperactivity and precocious maturation of corticostriatal circuits in Shank3B(-/-) mice Mice with Dab1 or Vldlr insufficiency exhibit abnormal neonatal vocalization patterns Premature changes in neuronal excitability account for hippocampal network impairment and autistic-like behavior in neonatal BTBR T+tf/J mice.Altered mGluR5-Homer scaffolds and corticostriatal connectivity in a Shank3 complete knockout model of autism.The parvalbumin/somatostatin ratio is increased in Pten mutant mice and by human PTEN ASD alleles.A novel anesthesia regime enables neurofunctional studies and imaging genetics across mouse strains PX-RICS-deficient mice mimic autism spectrum disorder in Jacobsen syndrome through impaired GABAA receptor trafficking Negative allosteric modulation of the mGluR5 receptor reduces repetitive behaviors and rescues social deficits in mouse models of autism.Genetic aspects of autism spectrum disorders: insights from animal models

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Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits.

http://www.wikidata.org/entity/Q29618411

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2011 nî lūn-bûn

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2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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Absence of CNTNAP2 leads to ep ...... core autism-related deficits.

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Absence of CNTNAP2 leads to ep ...... core autism-related deficits.

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Absence of CNTNAP2 leads to ep ...... core autism-related deficits.

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Absence of CNTNAP2 leads to ep ...... core autism-related deficits.

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J.CELL.2011.08.040

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Amos Gdalyahu

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Anatol Bragin

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Brett S Abrahams

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Edward I Herman

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Hongmei Dong

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Joel Almajano

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Joshua T Trachtenberg

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Kellen D Winden

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Lisa I Sonnenblick

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Peyman Golshani

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P2860

Caspr2, a new member of the neurexin superfamily, is localized at the juxtaparanodes of myelinated axons and associates with K+ channels

Advances in autism

Correction of fragile X syndrome in mice.

Linkage, association, and gene-expression analyses identify CNTNAP2 as an autism-susceptibility gene

Molecular cytogenetic analysis and resequencing of contactin associated protein-like 2 in autism spectrum disorders

A functional genetic link between distinct developmental language disorders

Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1

Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism

Autism genome-wide copy number variation reveals ubiquitin and neuronal genes

Neurophysiological and computational principles of cortical rhythms in cognition

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235-246

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10.1016/J.CELL.2011.08.040

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1

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Daniel Geschwind

Olga Peñagarikano

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51684596

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