GEO DataSets

Analysis of hind limb skeletal muscle from 4-week old dy3K/dy3K animals, which completely lack expression of laminin α2 chain. Mutations in the laminin alpha2 chain gene cause congenital muscular dystrophy type 1A (MDC1A). Results provide insight into molecular mechanisms underlying this disorder.

Organism:

Mus musculus

Type:

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

Platform:

GPL1261

Series:

GSE12049

6 Samples

Download data: CEL

(Submitter supplied) Mutations in the gene encoding laminin a2 chain cause congenital muscular dystrophy, MDC1A. In skeletal muscle, laminin a2 chain binds at least two receptor complexes; the dystrophin-glycoprotein complex and integrin a7b1. To gain insight into the molecular mechanisms underlying this disorder, we performed gene expression profiling of laminin a2 chain deficient mouse limb muscle. One of the down-regulated genes encodes a protein called calcium and integrin binding protein 2 (Cib2) whose expression and function is unknown. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3371

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) Laminin (merosin) deficient muscular dystrophy in dy/dy mouse diaphragm muscle, 8 weeks old Keywords: muscle, muscular dystrophy, laminin, merosin, diaphragm, mouse

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1778

Platform:

GPL339

8 Samples

Download data

Analysis of diaphragms of alpha2-laminin deficient dy/dy animals. Alpha-2 laminin is important in muscle cell attachment, and its deficiency underlies classical congenital muscular dystrophy. Results provide insight into the events that link alpha2-laminin deficiency with muscle fiber necrosis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 disease state sets

Platform:

GPL339

Series:

GSE3252

8 Samples

Download data

(Submitter supplied) Analysis of integrin alpha7 transgenic mice skeletal muscle transcription profiles comparing to wild type controls. Integrin alpha7 is the major laminin binding integrin in muscle cells. Enhancing its expression has been demonstrated to alleviate pathology in a murine model of Duchenne muscular dystrophy. Results of this study provide insights into the effects of increasing integrin alpha7 expression on skeletal muscle transcription and physiology in vivo. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3209

Platform:

GPL1261

6 Samples

Download data: CEL, CHP, EXP

(Submitter supplied) Analysis of C2C12 myoblast induced with tetracycline to enhance integrin alpha7 expression. Integrin alpha7 is the major laminin binding integrin in muscle cells. Enhancing its expression has been demonstrated to alleviate pathology in a murine model of Duchenne muscular dystrophy. Results of this study provide insights into the effects of increasing integirn alpha7 expression on muscle cells and possible side effects associate with enhancing integrin alpha7 in muscle cells. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL, CHP, EXP

Analysis of skeletal muscle from transgenic females overexpressing integrin alpha7. Enhancement of alpha7 integrin levels alleviates pathology in a Duchenne muscular dystrophy murine model. Results provide insight into effects of increased integrin alpha7 on skeletal muscle transcription in vivo.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 protocol sets

Platform:

GPL1261

Series:

GSE8313

6 Samples

Download data: CEL, CHP, EXP

(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