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Links from GEO DataSets

Items: 6

1.

Dystrophin-deficient and dystrophin and utrophin double-deficient mice crossed with mice with full-length hDMD genes

(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
Series
Accession:
GSE6790
ID:
200006790
2.

Extraocular, hindlimb, and cardiac muscles, comparison of dko and mdx mice (Porter lab)

(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
Series
Accession:
GSE1463
ID:
200001463
3.
Full record GDS2001

Utrophin/dystrophin-deficient double mutant and dystrophin-deficient mdx mutant skeletal muscles

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
DataSet
Accession:
GDS2001
ID:
2001
4.

Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for DMD

(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
Series
Accession:
GSE7187
ID:
200007187
5.
Full record GDS3398

Utrophin overexpression effect on dystrophin-deficient mdx skeletal muscles

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
DataSet
Accession:
GDS3398
ID:
3398
6.

Effect of Estrogen Receptor Beta Ligand on Gene Expression in Liver

(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
Series
Accession:
GSE93154
ID:
200093154
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Supplemental Content

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