Congenital heart disease in mice deficient for the DiGeorge syndrome region
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Identification of a novel nuclear localization signal in Tbx1 that is deleted in DiGeorge syndrome patients harboring the 1223delC mutationNeuronal migration abnormalities and its possible implications for schizophreniaConnecting teratogen-induced congenital heart defects to neural crest cells and their effect on cardiac functionHearing loss in a mouse model of 22q11.2 Deletion Syndrome.Unraveling the genetic architecture of copy number variants associated with schizophrenia and other neuropsychiatric disorders.Annual Research Review: Transgenic mouse models of childhood-onset psychiatric disorders.Temporally regulated traffic of HuR and its associated ARE-containing mRNAs from the chromatoid body to polysomes during mouse spermatogenesisA Synaptic Function Approach to Investigating Complex Psychiatric Diseases.Jun is required in Isl1-expressing progenitor cells for cardiovascular developmentXenopus: An emerging model for studying congenital heart disease.Genetic Models in Applied Physiology. Functional genomics in the mouse: powerful techniques for unraveling the basis of human development and disease.A defect in early myogenesis causes Otitis media in two mouse models of 22q11.2 Deletion Syndrome.Genotype and cardiovascular phenotype correlations with TBX1 in 1,022 velo-cardio-facial/DiGeorge/22q11.2 deletion syndrome patients.The mechanism of TGF-β signaling during palate development.Chromosome engineering in zygotes with CRISPR/Cas9.Aneuploidy: from a physiological mechanism of variance to Down syndrome.Thalamic miR-338-3p mediates auditory thalamocortical disruption and its late onset in models of 22q11.2 microdeletion.Tbx1, subpulmonary myocardium and conotruncal congenital heart defects.Transcription factors in parathyroid development: lessons from hypoparathyroid disorders.Cardiac outflow tract anomalies.The impact of genetics on future drug discovery in schizophrenia.SDF1-CXCR4 signaling: A new player involved in DiGeorge/22q11-deletion syndrome.Mitochondria in complex psychiatric disorders: Lessons from mouse models of 22q11.2 deletion syndrome: Hemizygous deletion of several mitochondrial genes in the 22q11.2 genomic region can lead to symptoms associated with neuropsychiatric disease.The 22q11 deletion: DiGeorge and velocardiofacial syndromes and the role of TBX1.Congenital heart disease and genetic syndromes: new insights into molecular mechanisms.Neural crest-specific removal of Zfhx1b in mouse leads to a wide range of neurocristopathies reminiscent of Mowat-Wilson syndrome.Cyp26 genes a1, b1 and c1 are down-regulated in Tbx1 null mice and inhibition of Cyp26 enzyme function produces a phenocopy of DiGeorge Syndrome in the chick.Variable immune deficiency related to deletion size in chromosome 22q11.2 deletion syndrome.
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Congenital heart disease in mice deficient for the DiGeorge syndrome region
description
article publié dans la revue scientifique Nature
@fr
scientific article published in Nature
@en
wetenschappelijk artikel
@nl
наукова стаття, опублікована в Nature у вересні 1999
@uk
name
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@en
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@nl
type
label
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@en
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@nl
prefLabel
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@en
Congenital heart disease in mice deficient for the DiGeorge syndrome region
@nl
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P1476
Congenital heart disease in mice deficient for the DiGeorge syndrome region
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P2093
Carattini-Rivera S
Lindsay EA
Rosenblatt HM
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P2888
P304
P356
10.1038/43900
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P577
1999-09-01T00:00:00Z
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1007642836