GEO DataSets

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) 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

(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) 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

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) Determination of gene expression changes in hindlimb muscle (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal ages 7, 14, 23, 28, 56, and 112. Keywords: time-course

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS639

Platform:

GPL81

36 Samples

Download data: CEL

Temporal analysis of hindlimb gastrocnemius/soleus muscle from dystrophin-deficient mdx mice, a Duchenne muscular dystrophy (DMD) model. Postnatal ages 7 to 112 days examined. Results provide insight into mechanisms of muscular dystrophy pathogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 6 age, 2 strain sets

Platform:

GPL81

Series:

GSE1025

36 Samples

Download data: CEL

(Submitter supplied) Time-course microarray data set of mdx and wild type mice ranging from 1-20 weeks of age Keywords: time-course

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL485

36 Samples

Download data

(Submitter supplied) Determination of gene expression changes in extraocular and hindlimb (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal day 56. 5 independent replicates/muscle group/strain. Keywords: parallel sample

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS703

Platform:

GPL32

20 Samples

Download data: CEL

Analysis of extraocular (EOM) and hindlimb (gastrocnemius/soleus) muscle in mdx (dystrophin-deficient; Duchenne muscular dystrophy model) mice at postnatal day 56.5. Highly specific changes observed between dystrophic (leg) and spared (EOM) muscle.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 strain, 2 tissue sets

Platform:

GPL32

Series:

GSE1472

20 Samples

Download data: CEL

(Submitter supplied) Transcriptome analysis of hindlimb muscles from dystrophic mice Muscular dystrophies (MD) are a clinically and genetically heterogeneous group of mendelian diseases. The underlying pathophysiology and phenotypic variability in each form are much more complex, suggesting the involvement of many other genes. Thus, here we studied the whole genome expression profile in muscles from three mice models for MD, at different time points: Dmdmdx, carrying a mutation in dystrophin gene, Largemyd-/- with mutation in Large and Dmdmdx/Largemyd-/- bearing both mutations. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

60 Samples

Download data: CEL, CHP

(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) 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

(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) We report RNA sequencing data from tibialis anterior muscles of 4 month old male wild type C57Bl/6 mice and mdx/mTR mice (generated in the C57Bl/6 background), which lack the dystrophin and telomerase RNA component genes.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

12 Samples

Download data: TXT

(Submitter supplied) ABSTRACT Stimulating the commitment of implanted dystrophin+ muscle derived stem cells (MDSC) into myogenic, as opposed to lipofibrogenic, lineages is a promising therapeutic strategy for Duchenne muscular dystrophy (DMD). To examine whether counteracting myostatin, a negative regulator of muscle mass and a pro-lipofibrotic factor, would help this process, we compared the in vitro myogenic and fibrogenic capacity of MDSC from wild type (WT), myostatin knockout (Mst KO), and mdx (DMD model) (mdx) young mice under various modulators, the expression of key stem cell and myogenic genes, and the capacity of these MDSC to repair the injured gastrocnemius in aged mdx mice with exacerbated lipofibrosis. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL13474

4 Samples

Download data: XLS

(Submitter supplied) Duchenne muscular dystrophy (DMD) is a progressive severe muscle-wasting disease caused by mutations in DMD encoding dystrophin that leads to loss of muscle function with cardiac/respiratory failure and premature death. Since dystrophic muscles are sensed by infiltrating inflammatory cells and gut microbial communities can cause immune dysregulation and metabolic syndrome, we sought to investigate whether intestinal bacteria may support the muscle immune response in mdx dystrophic animal model. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

20 Samples

Download data: TXT