Transcript level alterations reflect gene dosage effects across multiple tissues in a mouse model of down syndrome
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Primary and secondary transcriptional effects in the developing human Down syndrome brain and heartGene-dosage effects in Down syndrome and trisomic mouse modelsCell array-based intracellular localization screening reveals novel functional features of human chromosome 21 proteinsConcise review: new paradigms for Down syndrome research using induced pluripotent stem cells: tackling complex human genetic diseaseSubmicroscopic deletion in patients with Williams-Beuren syndrome influences expression levels of the nonhemizygous flanking genesChromosomal instability and cancer: a complex relationship with therapeutic potentialAneuploidy: cells losing their balanceCross-species hybridisation of human and bovine orthologous genes on high density cDNA microarraysHard-Wired Control of Bacterial Processes by Chromosomal Gene LocationMouse models of Down syndrome as a tool to unravel the causes of mental disabilitiesOlig1 and Olig2 triplication causes developmental brain defects in Down syndromeChromosome 21 and down syndrome: from genomics to pathophysiologyComprehensive behavioral phenotyping of Ts65Dn mouse model of Down syndrome: activation of β1-adrenergic receptor by xamoterol as a potential cognitive enhancer.The use of mouse models to understand and improve cognitive deficits in Down syndrome.A mouse model of Down syndrome trisomic for all human chromosome 21 syntenic regions.Effects of individual segmental trisomies of human chromosome 21 syntenic regions on hippocampal long-term potentiation and cognitive behaviors in mice.Expression evolution facilitated the convergent neofunctionalization of a sodium channel gene.Validation of microarray data in human lymphoblasts shows a role of the ubiquitin-proteasome system and NF-kB in the pathogenesis of Down syndrome.PCP4 (PEP19) overexpression induces premature neuronal differentiation associated with Ca(2+) /calmodulin-dependent kinase II-δ activation in mouse models of Down syndrome.Genetic dissection of the Down syndrome critical region.Discovery of novel serum biomarkers for prenatal Down syndrome screening by integrative data mining.Trisomy for the Down syndrome 'critical region' is necessary but not sufficient for brain phenotypes of trisomic mice.Cell type-specific over-expression of chromosome 21 genes in fibroblasts and fetal hearts with trisomy 21.Understanding the basis for Down syndrome phenotypes.Altered expression of mitochondrial and extracellular matrix genes in the heart of human fetuses with chromosome 21 trisomyProfiling expression changes caused by a segmental aneuploid in maize.Differential expression of genes mapping to recurrently abnormal chromosomal regions characterize neuroblastic tumours with distinct ploidy statusA mouse embryonic stem cell bank for inducible overexpression of human chromosome 21 genes.Detection of Copy Number Alterations Using Single Cell SequencingMeiotic behavior of aneuploid chromatin in mouse models of Down syndrome.Gene expression profiling in a mouse model identifies fetal liver- and placenta-derived potential biomarkers for Down Syndrome screening.Meta-analysis of heterogeneous Down Syndrome data reveals consistent genome-wide dosage effects related to neurological processesOhnologs in the human genome are dosage balanced and frequently associated with disease.Segmental trisomy of chromosome 17: a mouse model of human aneuploidy syndromesFunctional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networksTranscriptome-wide survey of mouse CNS-derived cells reveals monoallelic expression within novel gene families.Single cell sequencing reveals low levels of aneuploidy across mammalian tissues.Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.The App-Runx1 region is critical for birth defects and electrocardiographic dysfunctions observed in a Down syndrome mouse model.No Evidence for Mutations that Deregulate GARS-AIRS-GART Protein Levels in Children with Down Syndrome
P2860
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P2860
Transcript level alterations reflect gene dosage effects across multiple tissues in a mouse model of down syndrome
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Transcript level alterations r ...... a mouse model of down syndrome
@ast
Transcript level alterations r ...... a mouse model of down syndrome
@en
type
label
Transcript level alterations r ...... a mouse model of down syndrome
@ast
Transcript level alterations r ...... a mouse model of down syndrome
@en
prefLabel
Transcript level alterations r ...... a mouse model of down syndrome
@ast
Transcript level alterations r ...... a mouse model of down syndrome
@en
P2093
P2860
P50
P356
P1433
P1476
Transcript level alterations r ...... a mouse model of down syndrome
@en
P2093
Barbara Eppens
Daniela Balzereit
Gail Stetten
Marc Sultan
Marie-Laure Yaspo
Mathew T Pletcher
Matthias Steinfath
Nidhi G Saran
Roger H Reeves
Sarah T South
P2860
P304
P356
10.1101/GR.1951304
P577
2004-07-01T00:00:00Z