GEO DataSets

Analysis of muscle biopsy specimens from patients with various muscle diseases. Results provide insight into the diagnosis and pathogenesis of muscle diseases.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 11 disease state sets

Platform:

GPL97

Series:

GSE3307

119 Samples

Download data: CEL

(Submitter supplied) 49 human patient mRNA profiles was generated using HG-U133 Plus 2.0 microarrays. Procesed in Affymetrix Expression console using Plier normalization method and later processed in Partek Genomics Suite. The clustering figure was generated using HCE clustering software. We sought to determine the mechanisms underlying failure of muscle regeneration that is observed in dystrophic muscle through hypothesis generation using muscle profiling data (human dystrophy and murine regeneration). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

49 Samples

Download data: CEL

(Submitter supplied) Summary: Genetic disorders of muscle cause muscular dystrophy, and are some of the most common inborn errors of metabolism. Muscle also rapidly remodels in response to training and innervation. Muscle weakness and wasting is important in such conditions as aging, critical care medicine, space flight, and diabetes. Finally, muscle can also be used to investigate systemic defects, and the compensatory mechansisms invoked by cells to overcome biochemical and genetic abnormalities. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Datasets:

GDS1956 GDS2855

Platforms:

GPL97 GPL96

242 Samples

Download data: CEL

(Submitter supplied) Temporal expression profiling was utilized to define transcriptional regulatory pathways in vivo in a mouse muscle regeneration model. Potential downstream targets of MyoD were identified by temporal expression, promoter data base mining, and gel shift assays; Slug and calpain 6 were identified as novel MyoD targets. Slug, a member of the snail/slug family of zinc finger transcriptional repressors critical for mesoderm/ectoderm development, was further shown to be a downstream target by using promoter/reporter constructs and demonstration of defective muscle regeneration in Slug null mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS233 GDS234

Platforms:

GPL32 GPL81

66 Samples

Download data: CEL

Analysis of muscle biopsy specimens from patients with various muscle diseases. Results provide insight into the diagnosis and pathogenesis of muscle diseases.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 12 disease state sets

Platform:

GPL96

Series:

GSE3307

121 Samples

Download data: CEL

Cardiotoxin injected into gastrocnemius muscle to induce muscle regeneration. Muscles profiled at 27 time points (0-40 days) post-injection. Transcriptional regulatory pathways defined.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 27 time sets

Platform:

GPL81

Series:

GSE469

54 Samples

Download data: CEL

Cardiotoxin injected into mouse gastrocnemius muscle to induce muscle regeneration. Muscles profiled at 27 time points (0-40 days) post-injection. Transcriptional regulatory pathways defined.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 6 time sets

Platform:

GPL32

Series:

GSE469

12 Samples

Download data: CEL

(Submitter supplied) Lamins and transmembrane proteins within the nuclear envelope regulate nuclear structure and chromatin organization. Nuclear Envelope Transmembrane Protein 39 (Net39) is muscle nuclear envelope protein whose functions in vivo have not been explored. We show that mice lacking Net39 succumb to severe myopathy and juvenile lethality, with concomitant disruption in nuclear integrity, chromatin accessibility, gene expression and metabolism. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL17021 GPL19057

24 Samples

Download data: BEDGRAPH, BIGWIG

(Submitter supplied) Lamins and transmembrane proteins within the nuclear envelope are regulators of nuclear structure and chromatin organization. Nuclear Envelope Transmembrane Protein 39 (Net39) is a muscle-restricted nuclear envelope protein. We show that mice lacking Net39 succumb to severe myopathy and neonatal lethality, with concomitant disruption in nuclear integrity, chromatin accessibility, gene expression and metabolism. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

12 Samples

Download data: TXT

(Submitter supplied) Lamins and transmembrane proteins within the nuclear envelope are regulators of nuclear structure and chromatin organization. Nuclear Envelope Transmembrane Protein 39 (Net39) is a muscle-restricted nuclear envelope protein. We show that mice lacking Net39 succumb to severe myopathy and neonatal lethality, with concomitant disruption in nuclear integrity, chromatin accessibility, gene expression and metabolism. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

6 Samples

Download data: BEDGRAPH

(Submitter supplied) Lamins and transmembrane proteins within the nuclear envelope are regulators of nuclear structure and chromatin organization. Nuclear Envelope Transmembrane Protein 39 (Net39) is a muscle-restricted nuclear envelope protein. We show that mice lacking Net39 succumb to severe myopathy and neonatal lethality, with concomitant disruption in nuclear integrity, chromatin accessibility, gene expression and metabolism. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

6 Samples

Download data: BIGWIG

(Submitter supplied) The present research is devoted to the identification of gene(s) severely affected by EMD mutations, leading to striated muscle laminopathies and more specifically the cardiomyopathy. For this purpose, we developped a large-scale gene expression approach on heart and skeletal tissues from Emd KO mouse model. Keywords: disease state modification

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2884

Platform:

GPL1261

14 Samples

Download data: CEL

Analysis of hearts of mutants lacking EMD, a gene encoding an A-type lamin. Mutations in EMD cause X-linked Emery-Dreifuss muscular dystrophy (EDMD). Results provide insight into the molecular mechanisms involved in the development of cardiomyopathy in X-linked EDMD.

Organism:

Mus musculus

Type:

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

Platform:

GPL1261

Series:

GSE6399

14 Samples

Download data: CEL

(Submitter supplied) RNA sequencing was performed on proliferating and differentiating emerin-null myogenic progenitors expressing emerin and EDMD-causing emerin mutants to identify molecular pathways implicated in Emery-Dreifuss Muscular Dystrophy.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL23479

54 Samples

Download data: XLS

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Caenorhabditis elegans

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL18245 GPL13657

32 Samples

Download data

(Submitter supplied) Point mutations in nuclear structural protein lamin A produce rare, tissue-specific diseases called laminopathies. The introduction of a human Emery Dreifuss Muscular Dystrophy (EDMD)-inducing mutation (lamin A-Y45C) into C. elegans lamin (LMN-Y59C), recapitulates many EDMD phenotypes, and correlates with hyper-sequestration of heterochromatic arrays at the nuclear periphery. Using muscle-specific emerin Dam-ID, we also document the misorganization of endogenous chromatin in the LMN-Y59C mutant. more...

Organism:

Caenorhabditis elegans

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18245

8 Samples

Download data: TXT

(Submitter supplied) Point mutations in nuclear structural protein laminA produce rare and generally tissue-specific diseases called laminopathies. The introduction of a human Emery Dreifuss Muscular Dystrophy (EDMD)-inducing mutation (laminA-Y45C) into C. elegans lamin (LMN-Y59C), recapitulates many EDMD phenotypes, and results in hyper-sequestration of heterochromatic arrays at the nuclear periphery. Using muscle-specific Emerin Dam-ID we show that the LMN-Y59C mutation also leads to misorganization of endogenous chromatin. more...

Organism:

Caenorhabditis elegans

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13657

24 Samples

Download data: TXT

(Submitter supplied) Laminopathies are caused by mutations in components of the nuclear envelope (NE). While most NE components are widely expressed, laminopathies affect only a subset of tissues. However, the understanding of the molecular mechanisms that explain this phenomenon is still elusive. Here we have performed RNA-Seq analysis in adult C. elegans nematodes comparing gene expression in wild type and single and double mutants of two components of the NE, EMR-1 and LEM-2. more...

Organism:

Caenorhabditis elegans

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13776

9 Samples

Download data: TXT

(Submitter supplied) Laminopathies are caused by mutations in components of the nuclear envelope (NE). While most NE components are widely expressed, laminopathies affect only a subset of tissues. However, the understanding of the molecular mechanisms that explain this phenomenon is still elusive. Here we have performed a genome wide DamID analysis in adult C. elegans nematodes comparing the DNA association profile of two components of the NE, Lamin/LMN-1 and Emerin/EMR-1. more...

Organism:

Caenorhabditis elegans

Type:

Genome binding/occupancy profiling by genome tiling array

Platform:

GPL16504

12 Samples

Download data: PAIR

(Submitter supplied) Mutations in the inner nuclear membrane protein emerin cause muscular dystrophy. Current evidence suggests that the muscle wasting is related to defects in muscle progenitor cell differentiation and regeneration. We obtained miRNA and mRNA expression data from wildtype and emerin-null cells and looked at gene expression differences between them.

Organism:

Mus musculus; synthetic construct

Type:

Expression profiling by array; Non-coding RNA profiling by array

Platforms:

GPL8786 GPL1261

8 Samples

Download data: CEL, CHP