Analysis of Roquin targetome during HCMV infection
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE132081 | GEO | 2019/08/15
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of Roquin targetome during HCMV infection
| PRJNA545893 | ENA
Project description:To elucidate miRNA-mediated temporal crosstalk during productive infection, we identified genome-wide miRNA target sites using Argonaute-crosslinking and immunoprecipitation followed by high-throughput sequencing (AGO-CLIPseq) in human cytomegalovirus (HCMV)-infected cells and evaluated the targeting efficacy by applying our new AGO-CLIPseq enrichment (ACE)-scoring algorithm. To uncover the miRNA targetome in uninfected or infected human foreskin fibroblasts with HCMV (24, 48 and 72 post-infection hour) were subjected to take AGO-CLIPseq as well as mRNAseq/smallRNAseq.
2014-12-03 | E-GEOD-63797 | biostudies-arrayexpress
Project description:To elucidate miRNA-mediated temporal crosstalk during productive infection, we identified genome-wide miRNA target sites using Argonaute-crosslinking and immunoprecipitation followed by high-throughput sequencing (AGO-CLIPseq) in human cytomegalovirus (HCMV)-infected cells and evaluated the targeting efficacy by applying our new AGO-CLIPseq enrichment (ACE)-scoring algorithm.
2014-12-03 | GSE63797 | GEO
Project description:Small RNA deep sequencing analysis was conducted on primary human fibroblasts infected with human cytomegalovirus (HCMV). HCMV-encoded miRNAs accumulated to ~20% of the total smRNA population at late stages of infection, and our analysis led to improvements in viral miRNA annotations and identification of novel HCMV miRNAs. Through crosslinking and immunoprecipitation of Argonaute-bound RNAs from infected cells, followed by high-throughput sequencing (Ago CLIP-seq), we obtained direct evidence for incorporation of all HCMV miRNAs into the endogenous host silencing machinery. Additionally, significant upregulation was observed during infection for a host miRNA cluster containing miR-96, miR-182 and miR-183. We also identified novel non-miRNA forms of virus-derived smRNAs, revealing greater complexity within the smRNA population during HCMV infection. High-throughput profiling of smRNAs, Ago1-, and Ago2-associated miRNAs from HCMV-infected fibroblast cells. Wild-type HCMV Towne (Genbank FJ616285.1) was used for these studies.
2011-11-10 | E-GEOD-33584 | biostudies-arrayexpress
Project description:We have established that human cytomegalovirus (HCMV) infection modulates the biology of target primary blood monocytes, allowing HCMV to use monocytes as 'vehicles' for its systemic spread. HCMV infection of monocytes results in rapid induction of PI(3)K and NF-kB activity. Integrins, which are upstream of the PI(3)K and NF-kB pathways, were shown to be involved in HCMV binding to and entry into fibroblasts, suggesting that receptor-ligand-mediated signaling following viral binding to integrins on monocytes could trigger the functional changes seen in infected monocytes. We now show that integrin engagement and the activation of the integrin/Src-signaling pathway is essential for the induction of HCMV-infected monocyte motility. To investigate how integrin engagement by HCMV triggers monocyte motility, we examined the infected monocyte transcriptome and found that the integrin/Src-signaling pathway regulates the expression of paxillin, which is an important signal transducer in the regulation of actin rearrangement during cell adhesion and movement. Functionally, we observed that paxillin is activated via the integrin/Src-signaling pathway and is required for monocyte motility. Because motility is intimately connected to cellular cytoskeletal organization, a process that is also important in viral entry, we investigated the role paxillin regulation plays in the process of viral entry of monocytes. New results confirmed that HCMV`s ability to enter target monocytes is significantly inhibited in cells deficient in paxillin expression or that had their integrin/Src/paxillin signaling pathway blocked. From our data, HCMV-cell interactions emerge as an essential trigger for the cellular changes that allow for HCMV entry and hematogenous dissemination. Monocytes were mock-infected, HCMV-infected, or pretreated with PP2 inhibitor prior to HCMV infection. There were three samples analyzed per individual replicate. Three replicates are included. comparative studies with a use of the specific Src kinase activity inhibitor
2010-10-31 | E-GEOD-24238 | biostudies-arrayexpress
Project description:Small RNA deep sequencing analysis was conducted on primary human fibroblasts infected with human cytomegalovirus (HCMV). HCMV-encoded miRNAs accumulated to ~20% of the total smRNA population at late stages of infection, and our analysis led to improvements in viral miRNA annotations and identification of novel HCMV miRNAs. Through crosslinking and immunoprecipitation of Argonaute-bound RNAs from infected cells, followed by high-throughput sequencing (Ago CLIP-seq), we obtained direct evidence for incorporation of all HCMV miRNAs into the endogenous host silencing machinery. Additionally, significant upregulation was observed during infection for a host miRNA cluster containing miR-96, miR-182 and miR-183. We also identified novel non-miRNA forms of virus-derived smRNAs, revealing greater complexity within the smRNA population during HCMV infection.
2011-11-10 | GSE33584 | GEO
Project description:Infection of human fibroblasts with either human cytomegalovirus strain AD169 or a recombinant virus deleted for HCMV US17 Illumina HT-12 beadarrays were used to quantitate levels of host transcripts at either 12 or 96 hpi.
2013-11-30 | GSE50955 | GEO
Project description:Infection of human fibroblasts with either human cytomegalovirus strain AD169 or a recombinant virus deleted for HCMV US17 Illumina HT-12 beadarrays were used to quantitate levels of host transcripts at either 12 or 96 hpi. Cells were infected in biological triplicates at both 12 and 96 hours post infetion
2013-11-30 | E-GEOD-50955 | biostudies-arrayexpress
Project description:Human cytomegalovirus (HCMV) induces pro-inflammatory monocytes following infection and we have evidence that EGFR is a key mediator in this early activation. To begin to address how this signalling pathway is responsible for the rapid activation of infected monocytes, we examined the role this pathway played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of genes, including inflammatory genes, were regulated in a EGFR-dependent manner, identifying this pathway as a key cellular control point in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection. Keywords: Disease state To begin to globally define how EGFR is involved in the HCMV-induced changes in monocyte function, we performed a transcriptome analysis in the presence of inhibitors to the EGFR signalling pathway. Specifically, a cDNA microarray containing 12,625 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 24 hours post infection in the presence of blocking anti-EGFR antibody and pharmacological agent AG1478 (AG; an EGFR inhibitor). A total of 4 replicates from mock-infected, HCMV-infected, anti-EGFR antibody-pretreated infected and AG-pretreated infected monocytes were analyzed in this study.
2009-09-03 | E-GEOD-17948 | biostudies-arrayexpress
Project description:Human cytomegalovirus induces a pro-inflammatory monocyte following infection. To begin to address how HCMV induces these rapid changes in infected monocytes, we examined the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of pro-inflammatory genes were upregulated within 4 hours post infection. Experiment Overall Design: To begin to globally define the HCMV-induced changes in monocyte function, we performed a transcriptome analysis. Specifically, a cDNA microarray containing 12,626 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 4 hours post infection. A total of 6 replicates from mock-infected and 6 replicates from HCMV-infected monocytes were analyzed in this study.
2008-06-20 | E-GEOD-11408 | biostudies-arrayexpress