github link
Accession IconSRP074887

Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.

Organism Icon Mus musculus
Sample Icon 77 Downloadable Samples
Technology Badge IconIllumina HiSeq 2000

Submitter Supplied Information

Description
Huntington's disease (HD) is an inherited neurodegenerative disorder of which skeletal muscle atrophy is a common feature, and multiple lines of evidence support a muscle-based pathophysiology in HD mouse models. Inhibition of myostatin signaling increases muscle mass, and therapeutic approaches based on this are in clinical development. We have used a soluble ActRIIB decoy receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD. Transcriptional profiling of muscle in treated and untreated wild-type and R6/2 mice was performed to analyze the effect of the ActRIIB decoy on genes and pathways involved in maintaining normal muscle physiology as well as those dysregulated due to the mutant HTT gene mutation. Overall design: RNAseq was performed on tibialis muscle from wild-type, wildtype + decoy, R6/2 and R6/2 + decoy; N = 10 per group. RNAseq was done on an Illumina Hi-seq 2000. Paired-end sequencing was obtained, 4-plexed across lanes for a minimum of 38 million 50mer paired reads per sample
PubMed ID
Total Samples
80
Submitter’s Institution
No associated institution

Samples

Show of 0 Total Samples
Filter
Add/Remove
Accession Code
Title
Sex
Age
Specimen part
Cell line
Treatment
Subject
Processing Information
Additional Metadata
No rows found
Loading...