Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA155021 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE31745: Primary effusion lymphoma cell lines BC-1 and BC-3 GSE31746: BJAB Cell Lines Transduced with lentiviral vector pNL-SIN-CMV-AcGFP expressing KSHV miRNAs miR-K1, miR-K12-11, or miR-K4-3p GSE32109: microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina] Refer to individual Series
2011-11-16 | E-GEOD-32113 | biostudies-arrayexpress
Project description:BJAB cells were infected with pNL-SIN-CMV-AcGFP (see accession number GSE8867 for data) or pNL-SIN-CMV-AcGFP expressing KSHV miR-K1, miR-K12-11 or miR-K4-3p and sorted 48 hours after infection. 12 or 16 days after transduction, cytoplasmic RNA was harvested and gene expression analysis of independent BJAB cell pools was performed using Human Operon v3.0.2 arrays. Each sample was run against Universal Human Reference RNA, Stratagene. The samples listed here were processed in parallel to those with accession number GSE8867, which includes all matched control cell lines. 6 independent B cell pools each expressing KSHV miR-K1, miRK12-11, or miR-K4-3p are included. Matched controls include unmodified BJAB (3 arrays) and cells transducted with parental vector pNL-SIN-CMV-AcGFP (6 replicates).
2011-11-16 | E-GEOD-31746 | biostudies-arrayexpress
Project description:BJAB cells were infected with pNL-SIN-CMV-AcGFP (see accession number GSE8867 for data) or pNL-SIN-CMV-AcGFP expressing KSHV miR-K1, miR-K12-11 or miR-K4-3p and sorted 48 hours after infection. 12 or 16 days after transduction, cytoplasmic RNA was harvested and gene expression analysis of independent BJAB cell pools was performed using Human Operon v3.0.2 arrays. Each sample was run against Universal Human Reference RNA, Stratagene. The samples listed here were processed in parallel to those with accession number GSE8867, which includes all matched control cell lines.
2011-11-16 | GSE31746 | GEO
Project description:BJAB Cell Lines Unmodified, Transduced with ith lentiviral vector pNL-SIN-CMV-AcGFP or pNL-SIN-CMV-AcGFP/miR-K12-11
| PRJNA102233 | ENA
Project description:Transcriptional profiling of BJAB cells expressing miR-K12-9 and BCBL cells treated with miR-K12-9 inhibitor. To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs often display small reductions in their steady-state levels, perhaps as a result of their impaired translation. Accordingly, we examined cellular transcript accumulation by array-based expression profiling under four sets of conditions in which KSHV miRNAs were expressed or inhibited. Cells transfected with negative control miRNA compared to miR-K12-9 or negative miRNA inhibitor compared to miR-K12-9 inhibitor.
2012-11-01 | E-GEOD-40093 | biostudies-arrayexpress
Project description:Transcriptional profiling of BJAB cells expressing miR-K12-9 and BCBL cells treated with miR-K12-9 inhibitor. To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs often display small reductions in their steady-state levels, perhaps as a result of their impaired translation. Accordingly, we examined cellular transcript accumulation by array-based expression profiling under four sets of conditions in which KSHV miRNAs were expressed or inhibited.
2012-11-01 | GSE40093 | GEO
Project description:Transcriptional profiling of BJAB cells expressing miR-K12-6-5p. To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs often display small reductions in their steady-state levels, perhaps as a result of their impaired translation. Accordingly, we examined cellular transcript accumulation by array-based expression profiling under four sets of conditions in which KSHV miRNAs were expressed. Cells transfected with negative control miRNA compared to miR-K12-6-5p.
2015-02-11 | E-GEOD-65148 | biostudies-arrayexpress
Project description:All metazoan eukaryotes express microRNAs (miRNAs), ~22 nt long regulatory RNAs that can repress the expression of mRNAs bearing complementary sequences. Several DNA viruses also express miRNAs in infected cells, suggesting a role in viral replication and pathogenesis. While specific viral miRNAs have been shown to autoregulate viral mRNAs or downregulate cellular mRNAs via novel target sites, the function of the majority of viral miRNAs remains unknown. Here, we report that the miR-K12-11 miRNA encoded by Kaposi’s Sarcoma Associated Herpesvirus (KSHV) shows significant homology to cellular miR-155, including the entire miRNA “seed” region. Using a range of assays, we demonstrate that expression of physiological levels of miRK12- 11 or miR-155 results in the downregulation of an extensive set of common mRNA targets, including genes with known roles in cell growth regulation. Our findings indicate that viral miR-K12-11 functions as an ortholog of cellular miR-155 and has likely evolved to exploit a pre-existing gene regulatory pathway in B-cells. Moreover, the known etiological role of miR-155 in B-cell transformation suggests the possibility that miR-K12-11 may contribute to the induction of KSHV positive B-cell tumors in infected patients. BJAB cells were infected and sorted 48 hours after infection. 12 to 16 days after transduction, gene expression analysis of 10 independent BJAB cell pools, expressing AcGFP only or AcGPF and miR-K12-11, was performed using Human Operon v3.0.2 arrays. Each ample was run against Universal Human Reference RNA, Stratagene. # of Arrays: BJAB = 3 AcGFP only = 10 AcGFP miR-K12-11 = 11
2007-12-18 | E-GEOD-8867 | biostudies-arrayexpress
Project description:Transcriptional profiling of BJAB cells expressing miR-K12-6-5p. To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs often display small reductions in their steady-state levels, perhaps as a result of their impaired translation. Accordingly, we examined cellular transcript accumulation by array-based expression profiling under four sets of conditions in which KSHV miRNAs were expressed.
2015-02-11 | GSE65148 | GEO
Project description:Background: Kaposi’s sarcoma associated herpes virus (KSHV) is associated with tumors of endothelial and lymphoid origin. During latent infection, KSHV expresses miR-K12-11, an ortholog of the human tumor gene hsa-miR-155. Both gene products are microRNAs (miRNAs), which are important post-transcriptional regulators that contribute to tissue specific gene expression. Advances in target identification technologies and molecular interaction databases have allowed a systems biology approach to unravel the gene regulatory networks (GRNs) triggered by miR-K12-11 in endothelial and lymphoid cells. Understanding the tissue specific function of miR-K12-11 will help to elucidate underlying mechanisms of KSHV pathogenesis. Results: Ectopic expression of miR-K12-11 differentially affected gene expression in BJAB cells of lymphoid origin and TIVE cells of endothelial origin. Direct miRNA targeting accounted for a small fraction of the observed transcriptome changes: only 29 common genes were identified as putative direct targets of miR-K12-11 in both cell types. However, a number of commonly affected biological pathways, such as carbohydrate metabolism and interferon response related signaling, were revealed by gene ontology analysis. Integration of transcriptome profiling, bioinformatic algorithms, and databases of protein-protein interactome from the ENCODE project identified different nodes of GRNs utilized by miR-K12-11 in a tissue-specific fashion. These effector genes, including cancer associated transcription factors (TFs) and signaling proteins, amplified the regulatory potential of a single miRNA, from a small set of putative direct targets to a larger set of genes. Conclusions: This is the first comparative analysis of miRNA-K12-11’s effects in endothelial and B cells, from tissues infected with KSHV in vivo. MiR-K12-11 was able to broadly modulate gene expression in both cell types. Using a systems biology approach, we inferred that miR-K12-11 establishes its GRN by both repressing master TFs and influencing signaling pathways, to counter the host anti-viral response and to promote proliferation and survival of infected cells. The targeted GRNs are more reproducible and informative than target gene identification, and our approach can be applied to other regulatory factors of interest.
2014-07-15 | GSE59412 | GEO