EGAS00001001021-sc-20150422 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001001347 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Exome sequencing of a case of lethal EBV-driven LPD
| EGAS00001001021 | EGA
Project description:We aimed to decipher APOBEC3A driven mutational differences in human PDX_PDAC tissues. 40 human PDX_PDAC tissues were grouped based on their APOBEC3A expression levels into APOBEC3A High and Low groups. Illumina whole exome sequencing (WES) was performed and downstream variant analysis was applied.
2021-09-06 | E-MTAB-10115 | biostudies-arrayexpress
Project description:The raw data consist of whole exome sequencing data of cervical squamous samples
2022-02-11 | E-MTAB-11407 | biostudies-arrayexpress
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains genome-wide binding profile of the factor sc from E0-12 generated by ChIP and analyzed on Illumina Genome Analyzer. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf A validated dataset is comprised of three biological replicates for ChIP-chip experiments and two replicates for ChIP-seq and meet the modENCODE quality standards. The control sample is the chromatin Input used for ChIP. Most factors binding profiles are generated by using specific antibodies for the protein of interest. However, some factors have been tagged by GFP in a transgenic line. In that case, ChIP is generated using an anti-GFP antibody. This submission represents the ChIP-seq component of the study.
2011-12-16 | E-GEOD-34347 | biostudies-arrayexpress
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains genome-wide binding profile of the factor sc from E0-8 generated by ChIP and analyzed on Illumina Genome Analyzer. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf A validated dataset is comprised of three biological replicates for ChIP-chip experiments and two replicates for ChIP-seq and meet the modENCODE quality standards. The control sample is the chromatin Input used for ChIP. Most factors binding profiles are generated by using specific antibodies for the protein of interest. However, some factors have been tagged by GFP in a transgenic line. In that case, ChIP is generated using an anti-GFP antibody. This submission represents the ChIP-seq component of the study.
2011-12-28 | E-GEOD-34712 | biostudies-arrayexpress
Project description:Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma and immunosuppression-related lymphomas. These B-cell malignancies arise by distinct transformation pathways and utilize divergent viral and host expression programs. To identify host dependency factors elicited by EBV latent-infection states, we performed parallel genome-wide CRISPR/Cas9 screens in Burkitt lymphoma (BL) and lymphoblasotid cell lines (LCL). Our results highlighted 57 BL and 87 LCL genes selectively critical for their growth and survival. LCL hits were enriched for EBV-induced genes, including viral super-enhancer targets and multiple kinases. We uncovered key CD19/CD81 roles in EBV membrane protein-driven PI3K/AKT activation and mechanisms by which EBV evades tumor suppressor responses to its growth program. LMP1-induced cFLIP was critical for LCL defense against TNFa-mediated programmed cell death, while EBV-induced BATF/IRF4 were critical for LCL BIM suppression and MYC induction. EBV super-enhancer targeted IRF2 protected LCLs against BLIMP1 responses. Collectively, our results identify host/pathogen interaction-driven synthetic lethal targets for therapeutic intervention.
2017-05-11 | GSE93681 | GEO
Project description:We examined the viral epitranscriptome in EBV transformed lymphoblastoid cell lines (LcLs) and EBV-positive Burkitt's lymphoma, Akata cells, using methylated RNA immunoprecipitation followed by sequencing (MeRIP-seq). Biological replicates of ribo-RNA deleted mRNA of each cell type were prepared for MeRIP-seq followed by peak calling using the exome Peak package with settings for stringent peak calling on both strands of the genome.
2023-08-12 | GSE129217 | GEO
Project description:Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection. For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology. Multiple mice were either sham infected, infected with the seasonal H1N1 influenza A virus TX91 (10^6PFU), or infected with various sublethal or lethal doses of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 48h or 72h post infection. 5 different cell types were purified by flow sorting from lungs of individual animals and then processed to yield total RNA that was used for microarray analysis. The dataset contains 75 microarrays covering 25 experimental conditions with 3 biological replicates. This dataset is linked to a dataset containing 138 microarrays of whole lungs covering 20 experimental conditions.
2013-07-03 | E-GEOD-42639 | biostudies-arrayexpress
Project description:This study involves characterization of four head and neck cancer cell lines -- NT8e, OT9, AW13516 and AW8507, established from Indian head and neck cancer patients, using SNP arrays, whole exome and whole transcriptome sequencing.
2015-11-27 | E-MTAB-3961 | biostudies-arrayexpress
Project description:Identification of biological processes that distinguish lethal from non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity to during lethal influenza infection. For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology. Multiple mice were either sham infected, infected with the seasonal H1N1 influenza A virus TX91 (10^6PFU), or infected with various sublethal or lethal doses of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at various time points (24h, 48h, 72h and 240h post infection) and processed to yield whole lung RNA that was used for microarray analysis. The dataset contains 138 microarrays covering 20 experimental conditions with 7 biological replicates each. As an exception, the alternative non-infectious control condition (Alum treatment) contains 5 biological replicates. This dataset is linked to a dataset comparing the transcriptomes of 5 different cell types isolated from individual lungs of influenza A-infected or control animals (contains 75 microarrays covering 25 experimental conditions).
2013-07-03 | E-GEOD-42638 | biostudies-arrayexpress