Prion infected ScN2a and GT1
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1803 | GEO | 2005/08/24
SECONDARY ACCESSION(S): PRJNA90281
REPOSITORIES: GEO
Shared Molecules
Only show the datasets with similarity scores above: 0.5
Threshold
0.5
Similar Datasets
Project description:A comparison of prion infected and non-infected samples from neuroblastoma cells (N2a), and a comparison of prion infected and non-infected samples from hypothalmus cells (GT1). 11 dual-color DNA-chip hybridizations of cDNAs were made. Keywords: other
2010-06-09 | E-GEOD-1803 | biostudies-arrayexpress
Project description:The underlying pathogenic mechanisms of prion infection are not well characterized. To study the effect of prion infection on gene expression in neuronal cell cultures, a neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Large scale expression analysis was performed using a cDNA microarray chip comprising about 21,000 spotted ESTs. Over hundred genes were identified that are differentially expressed in 22L-infected cells when compared to uninfected cells. Several of the identified changes in gene expression have also been reported for other neurodegenerative diseases such as Alzheimer`s disease. Keywords: cDNA arrays, prion, N2a, neuroblastoma cell line, murine A neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Eight replicates including four dye swap experiments have been performed for the comparison of prion infected cells versus control cells.
2010-05-26 | E-GEOD-7119 | biostudies-arrayexpress
Project description:Cell culture models allow prion propagation studies ex vivo after contact with infectious brain homogenates. To date, among the neural cell lines, the mouse neuroblastoma-derived cell line N2a has been one of the most widely used model and has yet provided interesting insights into cell biology of prion propagation. Remarkably, persistently-infected N2a sublines have been set up and replicate prions without exhibiting any pathological changes. One further interesting feature of N2a is the possibility to establish by subcloning, sublines with a range of susceptibility to prions. Indeed, susceptible sublines propagate prions and accumulate the pathogenic isoform of the prion protein, PrPSc, at the opposite of resistant sublines. The aim of our study was to apply large-scale expression analysis using microarrays combined with quantitative real-time PCR to examine the gene expression profile in a persistently-infected N2a cell line, N2a58, infected with the mouse-adapted prion strain 22L, to seek for prion-specific gene transcription. We also questioned if we could observe identical variations of expression of these genes in three other 22L-infected N2a sublines. Finally, we examined the transcriptional state of a N2a subline considered as resistant when exposed to prions. Common pathways of gene transcription would disclose information on the molecular basis of the cell infection and help to identify potential therapeutic targets. Keywords: other
2009-07-07 | GSE5844 | GEO
Project description:The underlying pathogenic mechanisms of prion infection are not well characterized. To study the effect of prion infection on gene expression in neuronal cell cultures, a neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Large scale expression analysis was performed using a cDNA microarray chip comprising about 21,000 spotted ESTs. Over hundred genes were identified that are differentially expressed in 22L-infected cells when compared to uninfected cells. Several of the identified changes in gene expression have also been reported for other neurodegenerative diseases such as Alzheimer`s disease. Keywords: cDNA arrays, prion, N2a, neuroblastoma cell line, murine
2008-02-22 | GSE7119 | GEO
Project description:Prion diseases are rare, neurological disorders caused by the misfolding of the cellular prion protein (PrPC). The misfolded conformers aggregate into cytotoxic fibrils (PrPSc) that facilitate the conversion of additional prion proteins into their misfolded form. Intracellular PrPSc aggregates primarily accumulate within late endosomes and lysosomes, organelles that participate in the degradation and turnover of a large subset of the proteome. Thus, intracellular accumulation of PrPSc aggregates have the potential to globally influence protein degradation kinetics. We have analyzed the proteome-wide effect of prion infection on protein degradation rates in N2a neuroblastoma cells by dynamic stable isotopic labeling with amino acids in cell culture (dSILAC) and bottom-up proteomics to quantify the degradation rates of more than 4700 proteins in prion-infected and uninfected cells. As expected, the degradation rate of the prion protein is significantly decreased upon aggregation in infected cells. The data indicate that dilution due to cell division, rather than degradation, is the dominant factor in clearance of PrPSc in infected N2a cells. Conversely, the degradation kinetics of the remainder of the N2a proteome generally increases upon infection. This effect occurs concurrently with increases in the cellular activities of autophagy and lysosomal hydrolases. The resulting enhancement in proteome flux may play a role in the survival of N2a cells during prion infection.
2021-09-08 | PXD014577 | Pride
Project description:The neuroblastoma-derived cell line N2a is permissive to certain prion strains but resistant sublines unable to accumulate the pathological proteinase-K resistant form of the prion protein can be isolated. We compared for gene expression and phenotypes different N2a sublines that were susceptible or resistant to the 22L prion strain. Karyotypes and comparative genomic hybridization arrays revealed chromosomal imbalances but did not demonstrate a characteristic profile of genomic alterations linked to prion susceptibility. Likewise, we showed that this phenotype was not dependent on the binding of PrPres, the expression of the prion protein gene, or on its primary sequence. We completed this analysis by looking using real-time quantitative PCR at the expression of a set of genes encoding proteins linked to prion biology. None of the candidates could account by itself for the infection phenotype, nevertheless sublines had distinct transcriptional profiles. Taken together, our results do not support a role for specific genomic abnormalities and possible candidate proteins in N2a prion susceptibility. They also reveal genetic heterogeneity among the sublines and serve as a guidance for further investigation into the molecular mechanisms of prion infection.
2008-09-08 | GSE5374 | GEO
Project description:The neuroblastoma-derived cell line N2a is permissive to certain prion strains but resistant sublines unable to accumulate the pathological proteinase-K resistant form of the prion protein can be isolated. We compared for gene expression and phenotypes different N2a sublines that were susceptible or resistant to the 22L prion strain. Karyotypes and comparative genomic hybridization arrays revealed chromosomal imbalances but did not demonstrate a characteristic profile of genomic alterations linked to prion susceptibility. Likewise, we showed that this phenotype was not dependent on the binding of PrPres, the expression of the prion protein gene, or on its primary sequence. We completed this analysis by looking using real-time quantitative PCR at the expression of a set of genes encoding proteins linked to prion biology. None of the candidates could account by itself for the infection phenotype, nevertheless sublines had distinct transcriptional profiles. Taken together, our results do not support a role for specific genomic abnormalities and possible candidate proteins in N2a prion susceptibility. They also reveal genetic heterogeneity among the sublines and serve as a guidance for further investigation into the molecular mechanisms of prion infection. In a first approach, CGHa profiles were established for the parental cell line N2apcl, a sensitive (G9) and a resistant (F1) sublines, as compared to A/HeJ mouse strain normal DNA. To allow a more precise description of the differences between N2apcl and six of its derived sub-lines (58, D11, F1, G9, R4, R10), N2apcl DNA was used as reference DNA in a series of CGHa experiments, avoiding the potential copy number polymorphisms between the cell lines and A/HeJ murine DNAs.
2010-06-19 | E-GEOD-5374 | biostudies-arrayexpress
Project description:Analysis of GT1-7 cells treated with GnRH. In this dataset, we include the expression data obtained from GT1-7 cells after treatment with GnRH. We confirmed that GT1-7 cells expressed DUSP5 and DUSP6 after GnRH treatment. Results provide insight into the effect of GnRH on MAP kinase pathway.
2018-05-31 | GSE112857 | GEO
Project description:This report describes our study of the efficacy and the potential mechanism underlying the anti-prion action of a new anti-prion compound having a glycoside structure in prion-infected cells. The study revealed involvements of two factors in the mechanism of the compound action: interferon and a microtubule nucleation activator, phosphodiesterase 4D interacting protein. In particular, phosphodiesterase 4D interacting protein was suggested to be important in regulating the trafficking or fusion of prion protein-containing vesicles or structures in cells. The findings of the study are expected to be useful not only for the elucidation of cellular regulatory mechanisms of prion protein, but also for the implication of new targets for therapeutic development. Prion-infected N167 cells were treated with either anti-prion glycoside compound (Gly-9) or control glycoside compound (Gly-14) at a dose of 5 M-NM-<g/mL for three days. Then, gene expression profiles were analyzed by DNA microarray analysis. Experiments were performed in quadruplicate.
2014-02-22 | E-GEOD-55241 | biostudies-arrayexpress