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Links from GEO DataSets

Items: 20

1.

RNA-deep sequencing (RNA-Seq) analysis of dy2J/dy2J (Lama2-CMD mouse model), mdx (DMD mouse model) and Wild-type skeletal muscles

(Submitter supplied) Congenital muscular dystrophy type-1A (Lama2-CMD) and Duchenne Muscular dystrophy (DMD) result from deficiencies of laminin-α2 and dystrophin proteins, respectively. Although both proteins strengthen the sarcolemma, they are implicated in clinically distinct phenotypes. We used RNA-deep sequencing (RNA-Seq) of dy2J/dy2J, Lama2-CMD mouse model, skeletal muscle at 8 weeks of age to elucidate disease pathophysiology. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: XLS
Series
Accession:
GSE126416
ID:
200126416
2.

Time-course of mdx and wild type mice

(Submitter supplied) Time-course microarray data set of mdx and wild type mice ranging from 1-20 weeks of age Keywords: time-course
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL485
36 Samples
Download data
Series
Accession:
GSE1574
ID:
200001574
3.

Transcriptome analysis of Largemyd and Dmdmdx/Largemyd muscles in comparison to Dmdmdx: what make them different?

(Submitter supplied) Transcriptome analysis of hindlimb muscles from dystrophic mice Muscular dystrophies (MD) are a clinically and genetically heterogeneous group of mendelian diseases. The underlying pathophysiology and phenotypic variability in each form are much more complex, suggesting the involvement of many other genes. Thus, here we studied the whole genome expression profile in muscles from three mice models for MD, at different time points: Dmdmdx, carrying a mutation in dystrophin gene, Largemyd-/- with mutation in Large and Dmdmdx/Largemyd-/- bearing both mutations. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
60 Samples
Download data: CEL, CHP
Series
Accession:
GSE72151
ID:
200072151
4.

The mdx mutation in the 129/Sv background results in a milder phenotype: Transcriptome comparative analysis searching for the protective factors

(Submitter supplied) Transcriptome analysis of hindlimb muscles from dystrophic mice. The mdx mouse is a good genetic and molecular murine model for Duchenne Muscular Dystrophy (DMD), a progressive and devastating muscle disease. However, this model is inappropriate for testing new therapies due to its mild phenotype. Here, we transferred the mdx mutation to the 129/Sv strain with the aim to create a more severe model for DMD. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
22 Samples
Download data: CEL, CHP
Series
Accession:
GSE77126
ID:
200077126
5.

Extraocular and hindlimb muscle, comparison of wild type and mdx mice, 56 days (Porter lab)

(Submitter supplied) Determination of gene expression changes in extraocular and hindlimb (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal day 56. 5 independent replicates/muscle group/strain. Keywords: parallel sample
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS703
Platform:
GPL32
20 Samples
Download data: CEL
Series
Accession:
GSE1472
ID:
200001472
6.
Full record GDS703

Dystrophin-deficient mdx extraocular and leg muscle

Analysis of extraocular (EOM) and hindlimb (gastrocnemius/soleus) muscle in mdx (dystrophin-deficient; Duchenne muscular dystrophy model) mice at postnatal day 56.5. Highly specific changes observed between dystrophic (leg) and spared (EOM) muscle.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 strain, 2 tissue sets
Platform:
GPL32
Series:
GSE1472
20 Samples
Download data: CEL
DataSet
Accession:
GDS703
ID:
703
7.

Diaphram, comparison of wild type and mdx mice, 7 to 112 Days (Porter lab)

(Submitter supplied) Determination of gene expression changes in extraocular muscle of mdx (dystrophin-deficient) mice at postnatal ages 7, 14, 23, 28, 56, and 112 days. 3 independent replicates/age/strain. Data form part of publication: Human Molecular Genetics 13:257-269, 2004. Keywords = microarray Keywords = muscle Keywords: time-course
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS638
Platform:
GPL81
36 Samples
Download data: CEL
Series
Accession:
GSE1026
ID:
200001026
8.
Full record GDS638

Dystrophin-deficient mdx diaphram muscle development time course

Temporal analysis of diaphram muscle from dystrophin-deficient mdx mice, a Duchenne muscular dystrophy (DMD) model. Postnatal ages 7 to 112 days examined. Results provide insight into mechanisms of muscular dystrophy pathogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 6 age, 2 strain sets
Platform:
GPL81
Series:
GSE1026
36 Samples
Download data: CEL
DataSet
Accession:
GDS638
ID:
638
9.

Hindlimb muscle, comparison of wild type and mdx mice, 7 to 112 Day (Porter lab)

(Submitter supplied) Determination of gene expression changes in hindlimb muscle (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal ages 7, 14, 23, 28, 56, and 112. Keywords: time-course
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS639
Platform:
GPL81
36 Samples
Download data: CEL
Series
Accession:
GSE1025
ID:
200001025
10.

Extraocular muscle, comparison of wild type and mdx mice, 14 to 112 Days (Porter lab)

(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
Series
Accession:
GSE1008
ID:
200001008
11.
Full record GDS639

Dystrophin-deficient mdx hindlimb muscle development time course

Temporal analysis of hindlimb gastrocnemius/soleus muscle from dystrophin-deficient mdx mice, a Duchenne muscular dystrophy (DMD) model. Postnatal ages 7 to 112 days examined. Results provide insight into mechanisms of muscular dystrophy pathogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 6 age, 2 strain sets
Platform:
GPL81
Series:
GSE1025
36 Samples
Download data: CEL
DataSet
Accession:
GDS639
ID:
639
12.
Full record GDS614

Dystrophin-deficient mdx extraocular muscle development time course

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
DataSet
Accession:
GDS614
ID:
614
13.

Pax3 plays a role in Neuro-2a cells proliferation and neurite outgrowth

(Submitter supplied) Our fingdings suggested that Pax3 not only inhibited the cell viability and proliferation, but also affected the cell cycle and the neurite outgrowth of Neuro-2a cells.RNA sequencing analysis showed upregulated genes in Pax3 overexpressed group were involved in cell cycle machinery, which may reveal the potential mechanism of proliferation.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: XLS
Series
Accession:
GSE146058
ID:
200146058
14.

Partial resistance to HDAC inhibitors in FAPs of dystrophic muscles at late stages of disease is associated to epigenetic and transcriptional features of cellular senescence

(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
Platform:
GPL17021
36 Samples
Download data: FPKM_TRACKING
Series
Accession:
GSE189825
ID:
200189825
15.

Partial resistance to HDAC inhibitors in FAPs of dystrophic muscles at late stages of disease is associated to epigenetic and transcriptional features of cellular senescence [RNA-seq]

(Submitter supplied) Pharmacological treatment of Duchenne Muscular Dystrophy (DMD) with histone deacetylase inhibitors (HDACi) is currently being tested in clinical trials. Pre-clinical studies performed in mdx mice - the mouse model of DMD - have shown that HDACi promote compensatory muscle regeneration, while inhibiting fibro-adipogenic degeneration, by targeting fibro-adipogenic progenitors (FAPs); however, these beneficial effects are restricted to early stages of disease progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
24 Samples
Download data: FPKM_TRACKING
Series
Accession:
GSE189824
ID:
200189824
16.

Partial resistance to HDAC inhibitors in FAPs of dystrophic muscles at late stages of disease is associated to epigenetic and transcriptional features of cellular senescence [ChIP-seq]

(Submitter supplied) Pharmacological treatment of Duchenne Muscular Dystrophy (DMD) with histone deacetylase inhibitors (HDACi) is currently being tested in clinical trials. Pre-clinical studies performed in mdx mice - the mouse model of DMD - have shown that HDACi promote compensatory muscle regeneration, while inhibiting fibro-adipogenic degeneration, by targeting fibro-adipogenic progenitors (FAPs); however, these beneficial effects are restricted to early stages of disease progression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE189823
ID:
200189823
17.

DMD vs. AGING

(Submitter supplied) Comparative effects of Duchenne Muscular Dystrophy (DMD) and Aging in skeletal muscle Expression profiling established by microarray technology provides a powerful tool by which complex pathways can be assembled. The pathophysiology of Duchenne Muscular Dystrophy (DMD) is a complex process involving many pathways downstream of the primary genetic insult (lack of dystrophin). Similarly, the mechanisms implicated in muscle aging are only partially understood. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14713
16 Samples
Download data: GPR
Series
Accession:
GSE32720
ID:
200032720
18.

Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle

(Submitter supplied) The membrane protein Cripto plays a key role in shaping macrophage plasticity in skeletal muscle during regeneration and disease. Cripto acts as an extrinsic modulator of macrophage plasticity and is required for the proper expansion/maintenance of the CD206+ anti-inflammatory macrophage population. Nevertheless, Cripto deletion does not change the gene expression profile of F4/80+/Ly6CLow macrophages suggesting that Cripto was dispensable to induce/maintain the Ly6CLow phenotype.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE142072
ID:
200142072
19.

Enhanced skeletal muscle regeneration upon Bmi1 gain of function is driven by Mt1-mediated protection from oxidative stress.

(Submitter supplied) Three independently prepared satellite cell cultures isolated from STOPFloxBmi1 mice, treated with Adeno-Cre (A-Cre) infection and induced to differentiate for 2 days were analysed by whole-genome Illumina platform mouse v2 as compared to the same cells treated with Adeno-GFP (A-GFP).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE41878
ID:
200041878
20.

Decoding the transcriptome of muscular dystrophy using single-nucleus RNA sequencing

(Submitter supplied) Muscular dystrophy is a group of diseases that cause progressive weakness and degeneration of the skeletal muscles that control movement. Lacking polymerase I transcription release factor (PTRF, also known as Cavin1), an essential caveolae component, causes a secondary deficiency of caveolins resulting in muscular dystrophy. Because skeletal muscle is a heterogeneous tissue composed of different metabolic muscle fiber (myofibers) and mononuclear cells, the transcriptome responses of these myofibers and mononuclear cell to muscular dystrophy caused by PTRF deletion has not been explored. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE217390
ID:
200217390
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