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Expression data from C2C12 myotubes infected with RML prions

ABSTRACT: Prion infection in animals results in neurodegeneration and eventually death. To examine the cellular impact of Prion disease, we profiled non-proliferative fully differentiated C2C12 cells, which can replicate prions to high levels. Results suggest that accumulation of high levels of PrPSc in C2C12 myotubes does not cause any overt cellular dysfunction or molecular pathology.

ORGANISM(S): Mus musculus

PROVIDER: GSE44563 | GEO | 2013/12/22

SECONDARY ACCESSION(S): PRJNA190061

REPOSITORIES: GEO

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Expression data from C2C12 myotubes infected with RML prions

Project description:Prion infection in animals results in neurodegeneration and eventually death. To examine the cellular impact of Prion disease, we profiled non-proliferative fully differentiated C2C12 cells, which can replicate prions to high levels. Results suggest that accumulation of high levels of PrPSc in C2C12 myotubes does not cause any overt cellular dysfunction or molecular pathology. C2C12 cells were differentiated into confluent myotubes. Cells were infected or not with 100ul of 10% brain homogenate obtained from a C57BL/6 mouse clinically affected with RML prions. 16 days after infection, cells were collected by scraping and RML was purified.

2013-12-22 | E-GEOD-44563 | biostudies-arrayexpress

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circRNA expression in C2C12 myoblasts and myotubes

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Expression data from C2C12 myotubes treated with sugarcane top ethanolic extract (STEE) and control C2C12 myotubes.

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C2C12 Myotubes in response to Palmitate

Project description:To identify mediators of obesity-linked reductions in PGC-1, we tested the effects of cellular nutrients in C2C12 myotubes. While overnight exposure to high insulin, glucose, glucosamine, or amino acids had no effect, saturated fatty acids (FA) potently reduced PGC-1a and b mRNA expression. Keywords: Nutrient Effect

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Glucocorticoid receptor (GR) target genes in C2C12 myotubes

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Glucocorticoid receptor (GR) target genes in C2C12 myotubes

Project description:Analysis of C2C12 myotubes treated with dexamethasone (Dex) for 6 or 24 hours. Dex is a synthetic glucorticoid receptor agonist. Results provide insight to the effect of glucocorticoids on myotubes. C2C12 myotubes were cultured in DMEM supplemented with 2% horse serum, and treated with 1 u? Dex or an equal volume (0.01% v/v of media) of vehicle control ethanol for 6 or 24 hours. Total cellular RNA was isolated utilizing the NucleoSpin RNA II kit (Macherey-Nagel). RNA isolates were first quantified by standard spectrophotometry, and then qualitatively evaluated by capillary electrophoresis employing the Bio-Rad Experion system per manufacturer’s instruction. The final labeled cRNA samples were hybridized overnight to Illumina mouseWG-6 BeadChip arrays, which was performed at UCSF Genomic Core. All treatments were done in triplicates and the same batch of microarrays were used for all treatments. The Illumina expression arrays were pre-processed using lumi package. The differential expression analysis was performed using the Limma package.

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Gene expression profile of E1A infected C2C12 myotubes

Project description:Proliferating C2C12 myoblasts were induced to differentiate into myotubes and then infected with adenovirus expressing E1A (Ad-E1A), which induces cell cycle re-entry and dedifferentiation. We analyzed the transcriptional profile of E1A infected C2C12-myotubes through the Affymetrix Mouse Genome 430 2.0 Array, searching for genes that were significantly regulated between two independent biological replicates at two different time points (24h and 36h after infection with Ad-E1A). In addition, we took advantage of the E1A mutant known as YH47/dl928 (hereafter referred as YH47), which bears two mutations in the pocket-binding region of E1A (Y48H, C124G) able to disrupt the interaction with Rb and its cognate proteins and to impair cell-cycle re-entry phenotype. YH47 mutant was used to identify the Rb independent transcriptional reprogramming of C2C12. C2C12 cells were differentiated in vitro to myotubes as previously described. Myotubes were, then, infected with an adenovirus carrying the 12S form of E1A (dl520), with the YH47 E1A mutant (dl928) or with a control adenovirus (CTR) expressing a deletion of essentially the entire E1A gene (dl312). Two different time points after infection were considered (24 hours and 36 hours) to evaluate changes in C2C12 cells expression profile. Technical (A or B) and biological replicates (EXP1 or EXP2) were done for each condition.

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Genome-wide DNA methylation sequencing in C2C12 myoblasts and myotubes

Project description:We show the application of 5mC antibody-based methylated DNA immunoprecipitation followed sequencing technology for high-through profiling of DNA methylation in mouse C2C12 myoblasts and myotubes. By analyzing the methylation status of immunoprecipitated DNA fragments, we generated genome-wide DNA methyaltion maps in mouse C2C12 myoblasts and myotubes. We find that DNA methylation levels in myoblasts at rDNA promter and coding regions are higher than that in myotubes but not changed in intergenic regions.

2019-11-27 | GSE141047 | GEO

LaminB1 DamID in undifferentiated mouse C2C12 myoblasts (ATCC, Lot 59501261) and differentiated C2C12 myotubes

Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated C2C12 myoblasts (MBs) and 6 day differentiated C2C12 myotubes (MTs) using DamID with a Dam-Lamin B1-encoding lentivirus.

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