Gene expression variation in Down's syndrome mice allows prioritization of candidate genes

Abstract

Down's syndrome (DS), or trisomy 21, is a complex developmental disorder that exhibits many clinical signs that vary in occurrence and severity among patients. The molecular mechanisms responsible for DS have thus far remained elusive. We argue here that normal variation in gene expression in the population contributes to the heterogeneous clinical picture… (More)

DOI: 10.1186/gb-2007-8-5-r91

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Gene expression variation in Down's syndrome mice allows prioritization of candidate genes

Abstract

Topics

3 Figures and Tables

Cited By

Generation of a panel of antibodies against proteins encoded on human chromosome 21

Mental Retardation and Human Chromosome 21 Gene Overdosage: From Functional Genomics and Molecular Mechanisms Towards Prevention and Treatment of the Neuropathogenesis of Down Syndrome

A Comprehensive Diverse ‘-omics’ Approach to Better Understanding the Molecular Pathomechanisms of Down Syndrome

Down Syndrome: A Complex and Interactive Genetic Disorder

Systematic proteome and proteostasis profiling in human Trisomy 21 fibroblast cells

High throughput gene complementation screening permits identification of a mammalian mitochondrial protein synthesis (ρ(-)) mutant.

Neurogenetic Disorders of Down Syndrome and Potential Pharmacotherapies for Mental Retardation

Cognitive Enhancement

Long-term effects of neonatal treatment with fluoxetine on cognitive performance in Ts65Dn mice.

Express ion of Anthracyc l ine Reductases in Donors With and Without Down Syndrome

References

TotVar NE NEi ij j J i I = − = =

Common genetic variants account for differences in gene expression among ethnic groups

Alzheimer's disease and endocytic dysfunction: clues from the Down syndrome-related proteins, DSCR1 and ITSN1.

Analysis of pooled DNA samples on high density arrays without prior knowledge of differential hybridization rates

Defective cerebellar response to mitogenic Hedgehog signaling in Down [corrected] syndrome mice.

Expression profiling in primates reveals a rapid evolution of human transcription factors.

Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration

WI: Part I: clinical practice guidelines for children with Down syndrome from birth to 12 years

WI: Part II: clinical practice guidelines for adolescents and young adults with Down syndrome: 12 to 21 years

An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes.

Slides referencing similar topics

Gene expression variation in Down's syndrome mice allows prioritization of candidate genes

Abstract

Topics

3 Figures and Tables

Cited By

Generation of a panel of antibodies against proteins encoded on human chromosome 21

Mental Retardation and Human Chromosome 21 Gene Overdosage: From Functional Genomics and Molecular Mechanisms Towards Prevention and Treatment of the Neuropathogenesis of Down Syndrome

A Comprehensive Diverse ‘-omics’ Approach to Better Understanding the Molecular Pathomechanisms of Down Syndrome

Down Syndrome: A Complex and Interactive Genetic Disorder

Systematic proteome and proteostasis profiling in human Trisomy 21 fibroblast cells

High throughput gene complementation screening permits identification of a mammalian mitochondrial protein synthesis (ρ(-)) mutant.

Neurogenetic Disorders of Down Syndrome and Potential Pharmacotherapies for Mental Retardation

Cognitive Enhancement

Long-term effects of neonatal treatment with fluoxetine on cognitive performance in Ts65Dn mice.

Express ion of Anthracyc l ine Reductases in Donors With and Without Down Syndrome

References

TotVar NE NEi ij j J i I = − = =

Common genetic variants account for differences in gene expression among ethnic groups

Alzheimer's disease and endocytic dysfunction: clues from the Down syndrome-related proteins, DSCR1 and ITSN1.

Analysis of pooled DNA samples on high density arrays without prior knowledge of differential hybridization rates

Defective cerebellar response to mitogenic Hedgehog signaling in Down [corrected] syndrome mice.

Expression profiling in primates reveals a rapid evolution of human transcription factors.

Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration

WI: Part I: clinical practice guidelines for children with Down syndrome from birth to 12 years

WI: Part II: clinical practice guidelines for adolescents and young adults with Down syndrome: 12 to 21 years

An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes.

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