Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects - Test2 - elhamkhani - TriplyDB

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

http://www.wikidata.org/entity/Q21563377

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Genetics and Genomics of Congenital Heart Disease.The App-Runx1 region is critical for birth defects and electrocardiographic dysfunctions observed in a Down syndrome mouse model.The complex SNP and CNV genetic architecture of the increased risk of congenital heart defects in Down syndrome.Differentially expressed microRNAs in maternal plasma for the noninvasive prenatal diagnosis of Down syndrome (trisomy 21).A lacZ reporter gene expression atlas for 313 adult KOMP mutant mouse lines.DSCAM promotes refinement in the mouse retina through cell death and restriction of exploring dendrites.Deconstructing host-pathogen interactions in Drosophila.Systematic Tracking of Disrupted Modules Identifies Altered Pathways Associated with Congenital Heart Defects in Down Syndrome.An excess of deleterious variants in VEGF-A pathway genes in Down-syndrome-associated atrioventricular septal defects Generation of the Sotos syndrome deletion in mice.Overexpression of Down syndrome cell adhesion molecule impairs precise synaptic targeting Systems Genetics Approach Identifies Gene Pathways and Adamts2 as Drivers of Isoproterenol-Induced Cardiac Hypertrophy and Cardiomyopathy in Mice Genes and networks regulating cardiac development and function in flies: genetic and functional genomic approaches.Down Syndrome Cell Adhesion Molecule , Mother of Innovations.Down syndrome and the complexity of genome dosage imbalance.Biomechanics of early cardiac development.Dissecting the Role of the Extracellular Matrix in Heart Disease: Lessons from the Drosophila Genetic Model.Actionable mutations in canine hemangiosarcoma.Identification of COL6A2 mutations in progressive myoclonus epilepsy syndrome.DSCAM-mediated control of dendritic and axonal arbor outgrowth enforces tiling and inhibits synaptic plasticity.Drosophila in the Heart of Understanding Cardiac Diseases: Modeling Channelopathies and Cardiomyopathies in the Fruitfly.On the Morphology of the Drosophila Heart.In vivo bioassay to test the pathogenicity of missense human AIP variants.[Cardiac pathologies and aging: lessons from a tiny heart].Survey of Human Chromosome 21 Gene Expression Effects on Early Development in Danio rerio.

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

http://www.wikidata.org/entity/Q21563377

description

2011 nî lūn-bûn

@nan

2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի նոյեմբերին 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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name

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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type

label

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@ast

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@en

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@en-gb

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@nl

altLabel

Over-Expression of DSCAM and COL6A2 Cooperatively Generates Congenital Heart Defects

@en

prefLabel

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@ast

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

@en

Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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JOURNAL.PGEN.1002344

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Over-expression of DSCAM and COL6A2 cooperatively generates congenital heart defects

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Amir Gamliel

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Ethan Bier

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Julie R Korenberg

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Karen Ocorr

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Kirk L Peterson

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Michael G Rosenfeld

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Ouarda Taghli-Lamallem

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Robert J Wessells

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Rolf Bodmer

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P2860

Functional impact of global rare copy number variation in autism spectrum disorders

Transcript assembly and quantification by RNA-Seq reveals unannotated transcripts and isoform switching during cell differentiation

TopHat: discovering splice junctions with RNA-Seq

KCNQ potassium channel mutations cause cardiac arrhythmias in Drosophila that mimic the effects of aging.

DAVID: Database for Annotation, Visualization, and Integrated Discovery

Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources

Targeted gene expression as a means of altering cell fates and generating dominant phenotypes

Adult mice deficient in actinin-associated LIM-domain protein reveal a developmental pathway for right ventricular cardiomyopathy

S100A1 in cardiovascular health and disease: closing the gap between basic science and clinical therapy

Drosophila, an emerging model for cardiac disease

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10.1371/JOURNAL.PGEN.1002344

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2011-11-01T00:00:00Z

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22072978

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