Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse model of amyotrophic lateral sclerosis (ALS) vs. wild type


ABSTRACT: mRNA expression in the spinal cords of the G93A-SOD1 familial ALS transgenic mouse model was compared to that in nontransgenic (Normal mouse) and transgenic mice expressing wild-type (WT)SOD1. Gene Ontology (GO)analysis was used to characterize differences in expression between G93A-SOD1 mouse and nontransgenic mouse spinal cord. Changes in multiple GO categories were found. Many of these were associated with subsystems involving cell-cell communication and intracellular signal transduction. Expression profiles of mice expressing WT-SOD1 did not differ from nontransgenic mice. In contrast, protein profiling using proteomics technology indicated changes in mitochondrial protein expression in the G93A-SOD1 mouse spinal cord that were not found in the mRNA expression analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Lukas 

PROVIDER: E-GEOD-4390 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Informatics-assisted protein profiling in a transgenic mouse model of amyotrophic lateral sclerosis.

Lukas Thomas J TJ   Luo Wei Wei WW   Mao Haihong H   Cole Natalie N   Siddique Teepu T  

Molecular & cellular proteomics : MCP 20060329 7


One of the causes of amyotrophic lateral sclerosis (ALS) is due to mutations in Cu,Zn-superoxide dismutase (SOD1). The mutant protein exhibits a toxic gain of function that adversely affects the function of neurons in the spinal cord, brain stem, and motor cortex. A proteomic analysis of protein expression in a widely used mouse model of ALS was undertaken to identify differences in protein expression in the spinal cords of mice expressing a mutant protein with the G93A mutation found in human A  ...[more]

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