Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome profiling in knock-in mouse models of Huntington's disease [AllelicSeries_6month_TissueSurvey_mRNA]


ABSTRACT: Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 6 month old knock-in mice with CAG lengths of 175 along with littermate control wild-type animals. mRNA expression profiles were obtained via RNA-seq analysis performed on samples from the Brown Adipose tissue, White Adipose tissue around Gonad, White Adipose tissue around Intestine, Brain - Brainstem, Brain - Cerebellum, Brain - Hippocampus, Brain - Hypothalamus/Thalamus, Corpus callosum, Gastrocnemius, Heart, and Skin of 6 month old knock-in mice with CAG lengths of 175 along with littermate control wild-type animals.

ORGANISM(S): Mus musculus

SUBMITTER: Jeff Aaronson 

PROVIDER: E-GEOD-65775 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


To gain insight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths. We found repeat length-dependent transcriptional signatures to be prominent in the striatum, less so in cortex, and minimal in the liver. Coexpression network analyses revealed 13 striatal and 5 cortical modules that correlated highly with CAG length and age,  ...[more]

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