Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome. - Wikidata - wikimedia - TriplyDB

Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Neuronal and microglial regulators of cortical wiring: usual and novel guideposts Neuronal migration abnormalities and its possible implications for schizophrenia Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders Modeling a model: Mouse genetics, 22q11.2 Deletion Syndrome, and disorders of cortical circuit development Discovery of Rare Mutations in Autism: Elucidating Neurodevelopmental Mechanisms Increased stereotypy in conditional Cxcr4 knockout mice.Cortical interneurons require Jnk1 to enter and navigate the developing cerebral cortex.Early developmental disturbances of cortical inhibitory neurons: contribution to cognitive deficits in schizophrenia.Default mode network connectivity and reciprocal social behavior in 22q11.2 deletion syndrome.Phenotypic differences in hiPSC NPCs derived from patients with schizophrenia.Chemokine signaling in development and disease.Cognitive ability is associated with altered medial frontal cortical circuits in the LgDel mouse model of 22q11.2DS Chemokine receptors and cortical interneuron dysfunction in schizophrenia.Ranbp1, Deleted in DiGeorge/22q11.2 Deletion Syndrome, is a Microcephaly Gene That Selectively Disrupts Layer 2/3 Cortical Projection Neuron Generation.Cortical Morphology Differences in Subjects at Increased Vulnerability for Developing a Psychotic Disorder: A Comparison between Subjects with Ultra-High Risk and 22q11.2 Deletion Syndrome.BIG1 is required for the survival of deep layer neurons, neuronal polarity, and the formation of axonal tracts between the thalamus and neocortex in developing brain.The G protein-coupled receptor P2RY8 and follicular dendritic cells promote germinal center confinement of B cells, whereas S1PR3 can contribute to their dissemination Deficits in microRNA-mediated Cxcr4/Cxcl12 signaling in neurodevelopmental deficits in a 22q11 deletion syndrome mouse model Integrative mechanisms of oriented neuronal migration in the developing brain.Losing your inhibition: linking cortical GABAergic interneurons to schizophrenia.Cellular and molecular mechanisms controlling the migration of neocortical interneurons.Prenatal ontogeny as a susceptibility period for cortical GABA neuron disturbances in schizophrenia.Development of cortical interneurons Annual research review: Rare genotypes and childhood psychopathology--uncovering diverse developmental mechanisms of ADHD risk.Central nervous system niche involvement in the leukemia.Recurrent copy number variations as risk factors for neurodevelopmental disorders: critical overview and analysis of clinical implications.Using hiPSCs to model neuropsychiatric copy number variations (CNVs) has potential to reveal underlying disease mechanisms.Altered neurobiological function of brainstem hypoglossal neurons in DiGeorge/22q11.2 Deletion Syndrome.Abnormal gait, reduced locomotor activity and impaired motor coordination in Dgcr2-deficient mice.SDF1-CXCR4 signaling: A new player involved in DiGeorge/22q11-deletion syndrome.Identification of a sustained neurogenic zone at the dorsal surface of the adult mouse hippocampus and its regulation by the chemokine SDF-1 Structural abnormalities in cortical volume, thickness, and surface area in 22q11.2 microdeletion syndrome: Relationship with psychotic symptoms.Altered expression of developmental regulators of parvalbumin and somatostatin neurons in the prefrontal cortex in schizophrenia.The Cytokine CXCL12 Promotes Basket Interneuron Inhibitory Synapses in the Medial Prefrontal Cortex.Hippocampal GABAergic Inhibitory Interneurons.Cortical-amygdala volumetric ratios predict onset of symptoms of psychosis in 22q11.2 deletion syndrome.Distinct white-matter aberrations in 22q11.2 deletion syndrome and patients at ultra-high risk for psychosis.Cortical Development Requires Mesodermal Expression of Tbx1, a Gene Haploinsufficient in 22q11.2 Deletion Syndrome.Delays in GABAergic interneuron development and behavioral inhibition after prenatal stress.An Investigation of SDF1/CXCR4 Gene Polymorphisms in Autism Spectrum Disorder: A Family-Based Study.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

http://www.wikidata.org/entity/Q36389564

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

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Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome

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Anthony-Samuel LaMantia

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Daniel W Meechan

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P2860

Rethinking schizophrenia

Lhx6 activity is required for the normal migration and specification of cortical interneuron subtypes

Origins of cortical interneuron subtypes

TBX1 is responsible for cardiovascular defects in velo-cardio-facial/DiGeorge syndrome

The germinal zones of the basal ganglia but not the septum generate GABAergic interneurons for the cortex

Disordered connectivity in the autistic brain: Challenges for the ‘new psychophysiology’

Model of autism: increased ratio of excitation/inhibition in key neural systems

Cortical inhibitory neurons and schizophrenia

Autism spectrum disorders: developmental disconnection syndromes

Critical period plasticity in local cortical circuits

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Thomas M. Maynard

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