Transcriptomics

Dataset Information

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Transcription profiling of different types of skeletal muscles from wild type and alpha tropomyosin transgenic slow mice to investigate the molecular mechanisms implicated in the mouse model of nemaline myopathy.


ABSTRACT: The aim of this study was to investigate the molecular mechanisms implicated in this mouse model of nemaline myopathy, and to further compare the molecular disease response in different skeletal muscles. For this purpose, snap frozen skeletla muscle specimens from wild type and transgenic for alpha tropomyosin slow mice were studied. Five different muscle types were used (diaphragm, plantaris, extensor digitorum longus, tibialis anterior, gastrocnemus). Mice were sacrificed between 7 and 10 months. RNA pools from 3-5 animals were created and each pool was hybridized to a U74Av2 Affymetrix GeneChip. Datasets from 36 GeneChips were included in this study. Experiment Overall Design: 36 skeletal mouse muscle RNA pools were used, from 5 different skeletal muscles, in two different conditions (wild type and transgenic)

INSTRUMENT(S): 418 [Affymetrix]

ORGANISM(S): Mus musculus  

TISSUE(S): Plantaris, Gastrocnemius Muscle, Diaphragm, Extensor Digitorum Longus, Tibialis Anterior

DISEASE(S): Nemaline Myopathy,Normal

SUBMITTER: Despina Sanoudou  

PROVIDER: E-GEOD-3384 | ArrayExpress | 2007-12-01

SECONDARY ACCESSION(S): GDS2312GSE3384PRJNA93519

REPOSITORIES: GEO, ArrayExpress

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Publications

Skeletal muscle repair in a mouse model of nemaline myopathy.

Sanoudou Despina D   Corbett Mark A MA   Han Mei M   Ghoddusi Majid M   Nguyen Mai-Anh T MA   Vlahovich Nicole N   Hardeman Edna C EC   Beggs Alan H AH  

Human molecular genetics 20060728 17


Nemaline myopathy (NM), the most common non-dystrophic congenital myopathy, is a variably severe neuromuscular disorder for which no effective treatment is available. Although a number of genes have been identified in which mutations can cause NM, the pathogenetic mechanisms leading to the phenotypes are poorly understood. To address this question, we examined gene expression patterns in an NM mouse model carrying the human Met9Arg mutation of alpha-tropomyosin slow (Tpm3). We assessed five diff  ...[more]

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