Project description:C2C12 cell lines were genetically engineered to stably express WT human Desmin or the Desmin mutant R406W or I451M. Non-modified C2C12 cells were used as control. The goal was to determine the effect of different desmin mutation on the gene expression in a myoblast cell line.
Project description:ETFDH (electron transfer flavoprotein ubiquinone oxidoreductase) is a 64 kDa protein monomer located in the inner mitochondrial membrane, in charge of transferring the electrons received from the electron transfer flavoprotein ETF to the Coenzyme Q (Q). Pathological mutations in ETFDH lead to Multiple Acyl-CoA Dehydrogenase Deficiency (MADD; OMIM #231680). C2C12 cells lacking ETFDH were analysed by TMT analysis and compared to wt cells.
Project description:Transcriptional profiling of mouse myoblast cells comparing control vs. Mybbp1a knockdown. Stable clones of C2C12 cells harboring control or Mybbp1a-targeting shRNA were established and further pooled for analysis. Goal was to determine, based on the effects of Mybbp1a depletion on global gene expression, candidate downstream target genes of Mybbp1a, a putative transcriptional co-repressor.
Project description:We sought to determine the effects of over-expression of Gli1 on gene expression in C2C12 myotube cultures. C2C12 myoblasts were induced to differentiate for 4 days. At that time, when >80% of nuclei were incorporated into multi-nucleated syncitial myotubes, we infected the cultures with recombinant adenovirus expressing GFP alone or GFP and a full length human Gli1. Media was changed 12 hours later. Cultures were lysed 60 hours after the initial infection. Gli1 over-expression induces de-differentiation of myotubes and proliferation of myoblasts.
Project description:Transcriptomic changes induced by DUX4 expression were compared between human and mouse cell lines of muscle lineage. We used microarrays to compare transcripts induced in human rhabdmyosarcoma and mouse C2C12 cells ectopically expressing DUX4.
Project description:Transcriptional profiling of mouse myoblast cells comparing control vs. Mybbp1a knockdown. Stable clones of C2C12 cells harboring control or Mybbp1a-targeting shRNA were established and further pooled for analysis. Goal was to determine, based on the effects of Mybbp1a depletion on global gene expression, candidate downstream target genes of Mybbp1a, a putative transcriptional co-repressor. Two-condition experiment, control vs. Mybbp1a knockdown C2C12 cells (mixed stable clones). Biological replicates: 2.
Project description:Mutations in LMNA gene cause laminopathies in human. Mostly, laminopathies alter skeletal muscle tissue and lead to cardiomathy and lipodystrophy. We investigated the effect of mutations G232E (EDMD2 syndome) and R482L (FPLD2 syndrome) in LMNA gene on skeletal muclse functioning and metabolism using transgenic C2C12 myoblast cell lines and transcriptome analysis. We found abnormalities of nuclear lamina structure in mutant myoblasts, treir pro-myogenic commitment and metabolic disregulation on all stages of transgenic myoblasts differentiation.