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Links from GEO DataSets

Items: 20

1.
Full record GDS1956

Various muscle diseases (HG-U133A)

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
2.

Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy

(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
Series
Accession:
GSE109178
ID:
200109178
3.

Comparative profiling in 13 muscle disease groups

(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
Series
Accession:
GSE3307
ID:
200003307
4.

Temporal profiling in muscle regeneration.

(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
Series
Accession:
GSE469
ID:
200000469
5.
Full record GDS2855

Various muscle diseases (HG-U133B)

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
6.
Full record GDS234

Muscle regeneration (U74Av2)

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
7.
Full record GDS233

Muscle regeneration (U74Av1)

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
8.

The nuclear envelope protein Net39 is essential for muscle nuclear integrity and chromatin organization

(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
Series
Accession:
GSE154850
ID:
200154850
9.

The nuclear envelope protein Net39 is essential for nuclear integrity, chromatin organization, and muscle growth (RNA-Seq)

(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
Series
Accession:
GSE154849
ID:
200154849
10.

The nuclear envelope protein Net39 is essential for nuclear integrity, chromatin organization, and muscle growth (ChIP-Seq)

(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
Series
Accession:
GSE154848
ID:
200154848
11.

The nuclear envelope protein Net39 is essential for nuclear integrity, chromatin organization, and muscle growth (ATAC-Seq)

(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
Series
Accession:
GSE154847
ID:
200154847
12.

Comparison between gene expression in heart from Emd KO and control mice

(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
Series
Accession:
GSE6399
ID:
200006399
13.
Full record GDS2884

X-linked Emery-Dreifuss muscular dystrophy model and cardiomyopathy

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
DataSet
Accession:
GDS2884
ID:
2884
14.

EDMD-causing emerin mutant myogenic progenitors exhibit impaired differentiation using similar mechanisms

(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
Series
Accession:
GSE152226
ID:
200152226
15.

Loss of a heterochromatin anchor rescues altered genome organization and EDMD muscle defects triggered by a laminopathy mutation

(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
Series
Accession:
GSE136577
ID:
200136577
16.

RNA-seq: Loss of a heterochromatin anchor rescues altered genome organization and EDMD muscle defects triggered by a laminopathy mutation

(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
Series
Accession:
GSE136576
ID:
200136576
17.

DamID: Loss of a heterochromatin anchor rescues altered genome organization and EDMD muscle defects triggered by a laminopathy mutation

(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
Series
Accession:
GSE135850
ID:
200135850
18.

Next generation sequencing facilitates quantitative analysis of Caenorhabditis elegans N2 wild type, emr-1(gk119), lem-2(tm1582) and emr-1(RNAi) lem-2(tm1582) transcriptomes.

(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
Series
Accession:
GSE44682
ID:
200044682
19.

DamID of Dam::LMN-1 and Dam::EMR-1 in Caenorhabditis elegans adult worms

(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
Series
Accession:
GSE44188
ID:
200044188
20.

Expression data from H2K mouse myogenic precursor cells

(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
Series
Accession:
GSE31714
ID:
200031714
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