Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1146369 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:11,431 and 4,992 genes were determined in whole blood of healthy human volunteers and normal sheep, respectively following MPLA and LPS exposure Following the exposure 1,029 human and 175 sheep genes were differentially expressed. Of those 175 sheep genes, 54 had a known human ortolog. The major inflammatory mediators, such as IL-1-6-8, TNFa, NFkB, ETS2, PTGS2, PTX3, CXCL18, KYNU, and CLEC4E were similarly (>2-fold) upregulated in both human and sheep blood. Six healthy human volunteers and six normal sheep blood was incubated with LPS or MPLA for 90 minutes, then the blood was transferred to the Paxgene blood RNA tubes and the gene expression microarrays were scanned with G2556 Microaaray Scanner
2015-12-16 | E-GEOD-72558 | biostudies-arrayexpress
Project description:11,431 and 4,992 genes were determined in whole blood of healthy human volunteers and normal sheep, respectively following MPLA and LPS exposure Following the exposure 1,029 human and 175 sheep genes were differentially expressed. Of those 175 sheep genes, 54 had a known human ortolog. The major inflammatory mediators, such as IL-1-6-8, TNFa, NFkB, ETS2, PTGS2, PTX3, CXCL18, KYNU, and CLEC4E were similarly (>2-fold) upregulated in both human and sheep blood. Six healthy human volunteers and six normal sheep blood was incubated with LPS or MPLA for 90 minutes, then the blood was transferred to the Paxgene blood RNA tubes and the gene expression microarrays were scanned with G2556 Microaaray Scanner.
2015-12-16 | E-GEOD-72557 | biostudies-arrayexpress
Project description:Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. DNA copy number profiles generated with a new tool, ENCODER, were compared to DNA copy number profiles from SNP6, NimbleGen and low-coverage Whole Genome Sequencing.
2014-08-12 | GSE60254 | GEO
Project description:Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. Current methods for detection of copy number aberrations (CNA) from whole-exome sequencing (WES) data are based on the read counts of the captured exons only. However, accurate CNA determination is complicated by the non-uniform read depth and uneven distribution of exons. Therefore, we developed ENCODER (ENhanced COpy number Detection from Exome Reads), which eludes these problems. By exploiting the ‘off-target’ sequence reads, it allows for creation of robust copy number profiles from WES. The accuracy of ENCODER compares to approaches specifically designed for copy number detection, and outperforms current exon-based WES methods, particularly in samples of low quality. DNA copy number profiles generated with a new tool, ENCODER, were compared to DNA copy number profiles from SNP6, NimbleGen and low-coverage Whole Genome Sequencing.
2014-08-12 | GSE60168 | GEO
Project description:Visceral leishmaniasis (VL; Leishmania donovani) cases produce interferon- (IFN) and tumour necrosis factor (TNF) in response to soluble leishmanial antigen (SLA) in whole blood assays. These pro-inflammatory cytokines are crucial for activation of macrophages to kill L. donovani parasites. Detailed immunological studies comparing active with cured patients suggest that a balance exists between the pro-inflammatory cytokines TNF and IFN, and anti-inflammatory interleukin-10 (IL10). Our interest was to obtain a global understanding of the response to SLA in whole blood from active VL cases, and to determine what effect neutralising anti-IL10 would have on this response. Transcriptional profiles following SLA stimulation of whole blood from VL patients showed very few differentially expressed genes (DEGs), the majority belonging to a single network with TNF at the hub. In contrast, when anti-IL10 was added with SLA, hundreds of DEGs were observed, 65% belonging to a single network with TNF, IFNG, NFKBIA, IL6 and IL1B as hub genes in concert with a remarkable chemokine/cytokine storm. Our data demonstrate the singular impact of IL10 as a potent immune modulator in VL.
2021-03-31 | GSE146908 | GEO
Project description:Expression data from whole blood from healthy human individuals
| PRJNA616367 | ENA
Project description:T-cell prolymphocytic leukemia (T-PLL) is a rare disease with rapid clinical course. Whole-exome and whole-genome sequencing have identified structural alterations in T-PLL, including inversion, translocation and copy number variation. Epigenetic alterations are the hallmark of many cancers. However, genome-wide epigenomic profiles have not been reported in T-PLL. In this study, we generated genome-wide maps of regulatory regions in both T-PLL patients and healthy individuals using H3K4me3 and H3K27ac ChIP-seq. We revealed a global alteration of both promoter and enhancer landscape in T-PLL, which supported the role of epigenetic regulation in transcriptional dysregulation of oncogenes and genes involved in DNA damage response and T-cell activation.
2021-04-20 | GSE143374 | GEO