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Links from GEO DataSets

Items: 20

1.

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
2.
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
3.

Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2746
Platform:
GPL1261
21 Samples
Download data: CEL
Series
Accession:
GSE8000
ID:
200008000
4.

Comparison between gene expression in heart from Lmna H222P homozygous and control mice

(Submitter supplied) The present research is devoted to the identification of gene(s) severely affected by LMNA 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 Lmna H222P heterozygous Knock-In mouse model. Keywords: disease state modification
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
14 Samples
Download data: CEL
Series
Accession:
GSE6398
ID:
200006398
5.

Comparison between gene expression in heart from Lmna H222P heterozygous and control mice

(Submitter supplied) The present research is devoted to the identification of gene(s) severely affected by LMNA 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 Lmna H222P heterozygous Knock-In mouse model. Keywords: disease state modification
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
15 Samples
Download data: CEL
Series
Accession:
GSE6397
ID:
200006397
6.
Full record GDS2746

Lmna H222P homozygous and heterozygous mutant models of Emery-Dreifuss muscular dystrophy: hearts

Analysis of hearts of A-type lamin Lmna H222P homo-/heterozygous mutants. LMNA mutations lead to autosomal dominant and recessive Emery-Dreifuss muscular dystrophy which is characterized by dilated cardiomyopathy. Results provide insight into the role of LMNA in the development of cardiomyopathy.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 3 genotype/variation sets
Platform:
GPL1261
Series:
GSE8000
21 Samples
Download data: CEL
7.

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
8.
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
9.
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
10.

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
11.

transcriptomic data of soleus WT and Lmnap.H222P/H222P pre- and post-symptomatic mice

(Submitter supplied) The present research is devoted to the identification of gene(s) severely affected by LMNA mutations, leading to striated muscle laminopathies and more specifically the skeletal phenotype of Emery-Freifuss Muscular Dystrophy. For this purpose, we developed a large-scale gene expression approach on soleus skeletal tissues from wild type Lmna H222P homozygous Knock-In mouse mode at pre and post stages of the disease .
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
20 Samples
Download data: CEL
Series
Accession:
GSE146112
ID:
200146112
12.

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
13.

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
14.

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
15.

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
16.

Polycomb dysfunctional transcriptional repression in muscle stem cells contributes to lamin dependent muscular dystrophy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL17021
13 Samples
Download data: TXT, WIG
Series
Accession:
GSE123725
ID:
200123725
17.

Polycomb dysfunctional transcriptional repression in muscle stem cells contributes to lamin dependent muscular dystrophy [ChIP-seq]

(Submitter supplied) Polycomb group of proteins (PcG) and the nuclear Lamin A are key factors in the maintenance of chromatin higher order structures required for preserving cell identity. Mutations in the Lamin A/C gene cause several diseases, belonging to the class of laminopathies, including Emery-Dreifuss Muscular Dystrophy. Nevertheless, epigenetic mechanisms involved in the pathogenesis of lamin-dependent dystrophy are still largely unknown. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
7 Samples
Download data: WIG
Series
Accession:
GSE123724
ID:
200123724
18.

Polycomb dysfunctional transcriptional repression in muscle stem cells contributes to lamin dependent muscular dystrophy [RNA-seq]

(Submitter supplied) Polycomb group of proteins (PcG) and the nuclear Lamin A are key factors in the maintenance of chromatin higher order structures required for preserving cell identity. Mutations in the Lamin A/C gene cause several diseases, belonging to the class of laminopathies, including Emery-Dreifuss Muscular Dystrophy. Nevertheless, epigenetic mechanisms involved in the pathogenesis of lamin-dependent dystrophy are still largely unknown. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE123723
ID:
200123723
19.

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:
synthetic construct; Mus musculus
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
20.

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
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