Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Allen Herbst

PROVIDER: E-GEOD-44563 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Infectious prions accumulate to high levels in non proliferative C2C12 myotubes.

Herbst Allen A Banser Pamela P Velasquez Camilo Duque CD Mays Charles E CE Sim Valerie L VL Westaway David D Aiken Judd M JM McKenzie Debbie D

PLoS pathogens 20131107 11

Prion diseases are driven by the strain-specific, template-dependent transconformation of the normal cellular prion protein (PrP(C)) into a disease specific isoform PrP(Sc). Cell culture models of prion infection generally use replicating cells resulting in lower levels of prion accumulation compared to animals. Using non-replicating cells allows the accumulation of higher levels of PrP(Sc) and, thus, greater amounts of infectivity. Here, we infect non-proliferating muscle fiber myotube cultures ...[more]

PMID: 24244171

Similar Datasets

Transcriptomic Responses to Prion Disease in Rats

Project description:While prion infections have been extensively characterized in the laboratory mouse, little is known regarding the molecular responses to prions in other rodents. To explore these responses and make comparisons, we generated a prion disease in the laboratory rat by successive passage of mouse RML prions. Here we describe the accumulation of prions and associated pathology in the rat and describe the transcriptional impact throughout prion disease. Comparative transcriptional profiling between laboratory mice and rats suggests that similar molecular processes are unfolding in response to prion infection. At the level of individual transcripts, however, variability exists between mice and rats and many genes deregulated in mouse scrapie are not affected in rats. Notwithstanding these differences, many transcriptome responses are conserved between mice and rats infected with scrapie. Our findings highlight the usefulness of comparative approaches to understanding neurodegeneration and prion diseases in particular. We Adapted RML Mouse Scrapie into Rats and measured the resulting gene expression changes in brain as a result of disease progression. Rats were infected by intracranial inoculation with prion isolates obtained by adaptation of mouse RML scrapie prions into rats. Brain samples were collected from third and fourth passage infected rats and age-matched controls at specified timepoints and gene expression profiles obtained. For each time point, 3 diseased and control brain samples were profiled.

2015-09-01 | E-GEOD-63930 | biostudies-arrayexpress

Time course of prion infected (RML) and globular domain ligands (POM1) in cultured organotypic cerebellar slices (COCS)

Project description:Cultured organotypic cerebellar slices were exposed for different time points with either prions (RML) versus non-infectious brain homogenate (NBH) or ligands to the globular domain of the prion protein (POM1) vs IgG We used microarrays to characterize the temporal response of two inducers prion protein dependent cell death: COCS were exposed to RML prions or Non-infectious brain homogenate (NBH) and harvested after 14d, 25d, 38d and 45d (4 replicates each condition). COCS were exposed to POM1 or IgG and harvested after 8h, 1d, 3d, 7d, 10d (4 replicates each condition).

2015-01-22 | E-GEOD-65147 | biostudies-arrayexpress

Transcription profiling of mouse brain infected with prions in eight mouse-prion strain combinations in a systems approach to the study of prion disease

Project description:Prions cause transmissible neurodegenerative diseases and replicate by conformational conversion of normal, benign forms of prion protein (PrPC) to disease-causing PrPSc isoforms. A systems approach to disease postulates that disease arises from the pathological perturbation (genetic and/or environmental) of one or more biological networks in the relevant organ. In this regard, we tracked global (all mRNA transcripts) gene expression in the brains of eight distinct mouse strain-prion strain combinations at 8 - 10 time points throughout the progression of the disease to capture the effects of prion strain, host genetics, and PrP concentration on disease incubation time. Data are also available from http://prion.systemsbiology.net

2009-03-25 | E-MTAB-76 | biostudies-arrayexpress

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.

2013-12-22 | GSE44563 | GEO

Mus musculus

Project description:Expression data from C2C12 myotubes infected with RML prions

| PRJNA190061 | ENA

Time course of prion infected (RML) and globular domain ligands (POM1) in cultured organotypic cerebellar slices (COCS)

2015-01-22 | GSE65147 | GEO

Transcription profiling of mouse

Project description:Affymetrix genechip profiling analsysis (MOE430A and MOE430B) of murine neuroblastoma cells infected with either RML prion strain or mock brain homogenate Experiment Overall Design: Parental N2a cells were split into 6 aliquots, 3 of which were infected with RML prions and 3 of which were mock-infected with normal brain homogenate. There are three biological replicates in total for each experimental group.

2008-04-07 | E-GEOD-7229 | biostudies-arrayexpress

Transcriptomic Responses to Prion Disease in Rats

2015-09-01 | GSE63930 | GEO

Gene expression data from spleen, cervical spinal cord, and thalamic regions of ME7-inoculated mouse

Project description:An essential and remarkable process of the biochemical and physiological features in prion diseases is the conversion of a host-encoded prion protein (PrPC) into a misfolded isoform (PrPSc). The conversion of PrPC and the replication of prions, in cases of peripheral infection, occur following the uptake and subsequent spread of prions to brain via spinal cord. We investigated the changes of gene expression profiles in the spleen, cervical spinal cord and thalamus following intraperitoneal inoculation of ME7 scrapie prion and the inter-tissue alterations of the differentially expressed genes through Venn diagram to find genes which are commonly influenced by ME7 scrapie prion spread in the three tissues.

2021-12-31 | GSE157334 | GEO

Transcriptome analysis of peripheral lymphoid tissue immediately before and after the detection of PrPSc in sheep scrapie

Project description:Sheep scrapie is a transmissible spongiform encephalopathy (TSE), which are invariably fatal neurodegenerative diseases of the central nervous system (CNS). Accumulation of the misfolded prion protein, PrPSc in the CNS results in progressive neurodegenerative disease. For many transmissible spongiform encephalopathies (TSEs), peripheral lymphoid tissue is an important site of PrPSc amplification but without obvious immunological consequence. Susceptible VRQ homozygous New Zealand Cheviot sheep were infected with SSBP/1 scrapie by inoculation in the drainage area of the prescapular lymph nodes. PrPSc was consistently detected by immunohistology in these nodes at 50 days post infection (dpi). This study compares the genes and physiological pathways that are affected by the progression of TSE disease in the prescapular lymph nodes, focusing on time points immediately before (10 dpi) and after (50 dpi) the detection of disease-associated PrPSc.

2014-02-20 | E-MTAB-2327 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data