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Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome modulation analysis of cytomegalovirus-infected immature monocyte-derived dendritic cells

ABSTRACT: Analysis of dendritic cells (DCs) at 6h and 48h after infection with cytomegalovirus (CMV) versus non infected. CMV tends to induce immunosuppression followed by lasting immunity. DCs appear to play a role in this effect. Results provide insights into CMV/DC interactions and suggest mechanisms for CMV-regulated early immune response. Keywords: gene expression array-based, count In the present study, immature monocyte-derived dendritic cells were generated from CMV neg healthy blood donors and infected or not with an endotheliotropic CMV strain. Gene expression modulation by the CMV infection was studied in a time course assay (non-infected - NI - vs 6h or 48h post-infection. Patient C has no 48h sample

ORGANISM(S): Homo sapiens

SUBMITTER: Franck Halary

PROVIDER: E-GEOD-14490 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome modulation analysis of cytomegalovirus-infected immature monocyte-derived dendritic cells

Project description:Analysis of dendritic cells (DCs) at 6h and 48h after infection with cytomegalovirus (CMV) versus non infected. CMV tends to induce immunosuppression followed by lasting immunity. DCs appear to play a role in this effect. Results provide insights into CMV/DC interactions and suggest mechanisms for CMV-regulated early immune response. Keywords: gene expression array-based, count

2009-01-22 | GSE14490 | GEO

Transcription profiling of human monocyte derived LPS-activated activated dendritic cells treated with IL-10

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2008-06-16 | E-GEOD-9757 | biostudies-arrayexpress

Transcription profiling of human cells transfected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha 203/204/211E (3411E) for 48h

Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha mutant (ERalpha 203/204/211E) that functions exclusively at the ERE-independent pathway demonstrated that genomic responses assessed by microarrays from the ERE-independent pathway to E2-ERalpha are not sufficient to alter cellular growth, death or motility. These findings suggest that the ERE-dependent pathway is the canonical E2-ERalpha signaling in model cell lines. Experiment Overall Design: Cells were infected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha 203/204/211E (3411E) for 48h. Infected cells were then treated with 1 nM Estradiol 17beta for 6h. All experiments were repeated six independent times conducted at at six different days

2008-06-16 | E-GEOD-9758 | biostudies-arrayexpress

Transcription profiling of human ER negative cells response to estradiol-ERbeta and estradiol-ERbeta ERE binding defective mutant

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2008-06-15 | E-GEOD-6965 | biostudies-arrayexpress

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