GEO DataSets

Analysis of skeletal muscles from dystrophin-deficient mdx trangenics engineered to overexpress utrophin, a dystrophin-related protein. Dystrophin mutations result in Duchenne muscular dystrophy. mdx trangenics overexpressing utrophin display improved muscle function.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 3 strain sets

Platform:

GPL339

Series:

GSE7187

17 Samples

Download data: CEL

(Submitter supplied) Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse model of DMD can prevent dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3398

Platform:

GPL339

17 Samples

Download data: CEL

(Submitter supplied) Comparison by expression profiling of tissue from dKO (utrophin/dystrophin-deficient) and MDX mice at 8 weeks of age. Independent triplicate analyses/strain were done for extraocular, hindlimb, and cardiac muscle. Keywords = microarray Keywords = extraocular Keywords: parallel sample

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2001

Platform:

GPL81

18 Samples

Download data: CEL

Comparison of skeletal muscles of utrophin/dystrophin double knockout (dko) mutants and dystrophin-deficient mdx mutants. dko and mdx mutants display skeletal muscle weakness and degeneration but only dko mutants display clinical features similar to Duchenne muscular dystrophy patients.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation, 3 tissue sets

Platform:

GPL81

Series:

GSE1463

18 Samples

Download data: CEL

(Submitter supplied) Determination of gene expression changes in extraocular muscle of mdx (dystrophin-deficient) mice at postnatal ages 14, 28, 56, and 112 days. 3 independent replicates/age/strain. Keywords = microarray Keywords = muscle Keywords: time-course

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS614

Platform:

GPL81

24 Samples

Download data: CEL

Analysis of extraocular muscle (EOM) from dystrophin-deficient mdx mice, a Duchenne muscular dystrophy (DMD) model. Postnatal ages 14, 28, 56, and 112 days examined. EOM is unaffected in DMD, so results provide insight into mdx EOM protective mechanisms.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 4 age, 2 strain sets

Platform:

GPL81

Series:

GSE1008

24 Samples

Download data: CEL

(Submitter supplied) C57BL/6 male mice were fed with normal diet or high fat diet and treated with vehicle or 30 mg/kg/day s.c. of ER-beta ligand, B-LGND2. Genes differentially expressed by H.F.D. and B-LGND2 are represented in this RNA-Sequencing data

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16331

9 Samples

Download data: TSV

(Submitter supplied) In this study, Pax7-Cre mediated inactivation of Sirt6 in mdx mice resulted in profound improvement of the mdx phenotype at the functional level. To study the underlying molecular mechanisms and identify specific Sirt6 targets irrespectively to mdx mutation, we performed RNA-seq of freshly isolated muscle stem cells from control and Sirt6mKO mice.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

6 Samples

Download data: TXT

(Submitter supplied) In this study, Pax7-Cre mediated inactivation of Sirt6 in mdx mice resulted in profound improvement of the mdx phenotype at the functional level. To study the underlying molecular mechanisms we performed RNA-seq of muscles from control, mdx and Sirt6mKO/mdx mice.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

9 Samples

Download data: TXT

(Submitter supplied) In this study, Pax7-Cre mediated inactivation of Sirt6 in mdx mice resulted in profound improvement of the mdx phenotype at the functional level. To study the underlying molecular mechanisms we performed RNA-seq of MuSCs from control, mdx and Sirt6mKO/mdx mice.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18635

6 Samples

Download data: TXT

(Submitter supplied) Despite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The present experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology, despite the absence of a functional dystrophin protein. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS236

Platform:

GPL81

10 Samples

Download data: CEL

Examination of mdx mouse, Duchenne muscular dystrophy model. 16 week regenerating mdx muscle analyzed in search for salvage pathways that maintain skeletal muscle integrity in the absence of functional dystrophin protein.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 strain sets

Platform:

GPL81

Series:

GSE466

10 Samples

Download data: CEL

(Submitter supplied) Crossing of hDMD mice that contain the full-length 2.3 Mb hDMD gene were crossed with dystrophin-deficient mdx mice and dystrophin and utrophin double-deficient mdx x utrn-/- mice resulted in a full rescue of the dystrophic features of these mice, as concluded from histological analysis. Analysis on Affymetrix gene chips demonstrated that also expression profiles of the dystrophic mice were normalized by crossing with transgenic hDMD mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL81

9 Samples

Download data: CEL