Cleft palate in mice with a targeted mutation in the gamma-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67 - Wikidata - awgldk - TriplyDB

Cleft palate in mice with a targeted mutation in the gamma-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67

Cleft palate in mice with a targeted mutation in the gamma-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67

http://www.wikidata.org/entity/Q36597021

about

Pathogenesis of peroxisomal deficiency disorders (Zellweger syndrome) may be mediated by misregulation of the GABAergic system via the diazepam binding inhibitor GABAergic interneuron origin of schizophrenia pathophysiology.Dynamic expression of a glutamate decarboxylase gene in multiple non-neural tissues during mouse development Homozygosity for a missense mutation in the 67 kDa isoform of glutamate decarboxylase in a family with autosomal recessive spastic cerebral palsy: parallels with Stiff-Person Syndrome and other movement disorders Molecular basis of cleft palates in mice Transcriptional regulation of GAD1 GABA synthesis gene in the prefrontal cortex of subjects with schizophrenia Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks GABAergic neurons regulate lateral ventricular development via transcription factor Pax5 Growth hormone biases amygdala network activation after fear learning Metabolic distinction between vesicular and cytosolic GABA in cultured GABAergic neurons using 13C magnetic resonance spectroscopy.Cleft palate is caused by CNS dysfunction in Gad1 and Viaat knockout mice.Cleft lip and palate genetics and application in early embryological development.Mutation of the Drosophila vesicular GABA transporter disrupts visual figure detection.Two distinct mechanisms target GAD67 to vesicular pathways and presynaptic clusters Demonstration of functional coupling between gamma -aminobutyric acid (GABA) synthesis and vesicular GABA transport into synaptic vesicles The physiological roles of vesicular GABA transporter during embryonic development: a study using knockout mice.Mice lacking Gad2 show altered behavioral effects of ethanol, flurazepam and gabaxadol.Down-regulation of dendritic spine and glutamic acid decarboxylase 67 expressions in the reelin haploinsufficient heterozygous reeler mouse.Increased anxiety and altered responses to anxiolytics in mice deficient in the 65-kDa isoform of glutamic acid decarboxylase.Glutamate acid decarboxylase 1 promotes metastasis of human oral cancer by β-catenin translocation and MMP7 activation.NF-kappaB/Rel regulates inhibitory and excitatory neuronal function and synaptic plasticity.Retinoic acid, GABA-ergic, and TGF-beta signaling systems are involved in human cleft palate fibroblast phenotype Deletion of GAD67 in dopamine receptor-1 expressing cells causes specific motor deficits Orofacial clefting: recent insights into a complex trait Overexpression of Glutamate Decarboxylase in Mesenchymal Stem Cells Enhances Their Immunosuppressive Properties and Increases GABA and Nitric Oxide Levels.The role of the synthetic enzyme GAD65 in the control of neuronal gamma-aminobutyric acid release.In vivo knockdown of GAD67 in the amygdala disrupts fear extinction and the anxiolytic-like effect of diazepam in mice.Isolated cleft palate in mice with a targeted mutation of the LIM homeobox gene lhx8 Central nervous system effects of prenatal selective serotonin reuptake inhibitors: sensing the signal through the noise.Palmitoylation cycles and regulation of protein function (Review).Current concepts in genetics of nonsyndromic clefts DNA methyltransferases1 (DNMT1) and 3a (DNMT3a) colocalize with GAD67-positive neurons in the GAD67-GFP mouse brain.Vesicular and plasma membrane transporters for neurotransmitters.The spatiotemporal segregation of GAD forms defines distinct GABA signaling functions in the developing mouse olfactory system and provides novel insights into the origin and migration of GnRH neurons.The dynamics of GABA signaling: Revelations from the circadian pacemaker in the suprachiasmatic nucleus.Establishment of a molecular embryonic stem cell developmental toxicity assay.Local GABA circuit control of experience-dependent plasticity in developing visual cortex.Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression.The hydrophilic isoform of glutamate decarboxylase, GAD67, is targeted to membranes and nerve terminals independent of dimerization with the hydrophobic membrane-anchored isoform, GAD65.Increased expression of GAD65 and GABA in pancreatic beta-cells impairs first-phase insulin secretion.

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P2860

Cleft palate in mice with a targeted mutation in the gamma-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67

http://www.wikidata.org/entity/Q36597021

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1997 nî lūn-bûn

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Cleft palate in mice with a ta ...... glutamic acid decarboxylase 67

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Cleft palate in mice with a ta ...... glutamic acid decarboxylase 67

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Cleft palate in mice with a ta ...... glutamic acid decarboxylase 67

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Cleft palate in mice with a ta ...... glutamic acid decarboxylase 67

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Cleft palate in mice with a ta ...... glutamic acid decarboxylase 67

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B G Condie

http://www.w3.org/2001/XMLSchema#string

D I Gottlieb

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G Bain

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M R Capecchi

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P2860

Null mutation of Dlx-2 results in abnormal morphogenesis of proximal first and second branchial arch derivatives and abnormal differentiation in the forebrain

Mice devoid of gamma-aminobutyrate type A receptor beta3 subunit have epilepsy, cleft palate, and hypersensitive behavior

Mice homozygous for a targeted disruption of Hoxd-3 (Hox-4.1) exhibit anterior transformations of the first and second cervical vertebrae, the atlas and the axis

Derivation of completely cell culture-derived mice from early-passage embryonic stem cells

Site-directed mutagenesis by gene targeting in mouse embryo-derived stem cells

Molecular Identification of the 62 kd Form of Glutamic Acid Decarboxylase from the Mouse.

Two genes encode distinct glutamate decarboxylases.

Involvement of GABAA receptors in the outgrowth of cultured hippocampal neurons.

gamma-Aminobutyric acid outside the mammalian brain.

GABA and glutamate depolarize cortical progenitor cells and inhibit DNA synthesis.

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