GEO DataSets

(Submitter supplied) Mitochondrial diseases are a heterogeneous group of monogenic disorders that result from impaired oxidative phosphorylation (OXPHOS). As neuromuscular tissues are highly energy-dependent, mitochondrial diseases often affect skeletal muscle. Although genetic and bioenergetic causes of OXPHOS impairment in human mitochondrial myopathies are well established, there is a limited understanding of metabolic drivers of muscle degeneration. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

32 Samples

Download data: TXT

(Submitter supplied) Global gene expression analysis was performed comparing human skeletal muscle samples from patients with various forms of muscular dystrophy and mitochondrial myopathies in order to identify specific gene expression changes associated with collagen VI deficiency (leading to Ullrich´s Congenital Muscular Dystrophy) and depletion of mitochondrial DNA relative to other mitochondrial myopathies

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13607

29 Samples

Download data: TXT

(Submitter supplied) Analysis of gene expression in both muscle and liver due to the lost of one copy of the gene ADCK2. Heterocygous mouse ADCK2(+/-) present an altered gene expression that explain the adult phenotype, including myopathy in muscle and steatosis and inflamation in liver.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

20 Samples

Download data: TXT

(Submitter supplied) Skeletal muscle mitochondrial dysfunction is secondary to T2DM and can be improved by long-term regular exercise training Mitochondrial dysfunction has long been implicated to play a causative role in development of type 2 diabetes (T2DM). However, a growing number of recent studies provide data that mitochondrial dysfunction is a consequence of T2DM development. The aim of our study is to clarify in further detail the causal role of mitochondrial dysfunction in T2DM by a comprehensive ex vivo analysis of mitochondrial function combined with global gene expression analysis in muscle of pre-diabetic newly diagnosed untreated T2DM subjects and long-standing insulin treated T2DM subjects compared with age- and BMI-matched controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS3880

Platform:

GPL570

42 Samples

Download data: CEL

Analysis of skeletal muscle biopsies from insulin-treated type 2 diabetes (T2D) subjects before/after exercise training, pre-diabetics and healthy controls. Results provide insight into the molecular basis of T2D, the role of mitochondrial dysfunction, and the effects of prolonged exercise training.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 3 disease state, 34 individual, 3 protocol sets

Platform:

GPL570

Series:

GSE19420

42 Samples

Download data: CEL

(Submitter supplied) Purpose: We examined the impact of niacin on muscle gene expression in mitochondrial myopathy patients and healthy controls. Methods: Muscle transcriptomics profiles were generated using global transcriptomics analysis by RNA sequencing which was performed by the Beijing Genomic Institute (BGI) using their standard protocols Results: The pathway enrichment analysis of RNA-sequencing data indicated that phagosome formation, serine/glycine/one-carbon pathways (de novo serine biosynthesis, purine degradation, glutathione metabolism), LXR/RXR activation, eicosanoid, glycoprotein 6, atherosclerosis, iron homeostasis and cAMP-mediated signalling pathways were among the most significantly changed in patients. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL23227

29 Samples

Download data: CSV, TSV, TXT

(Submitter supplied) Analysis of muscle from C57BL/6 mice expressing V338Y mutant mitochondrial ribosomal protein.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

15 Samples

Download data: TXT