Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Dual transcriptomic analysis of HSV1 infected primary human fibroblasts (HFFF) in the presence and absence of VP22

PROVIDER: PRJNA505045 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8186990_1.fastq.gz	Fastqsanger.gz
	SRR8186990_2.fastq.gz	Fastqsanger.gz
	SRR8187000_1.fastq.gz	Fastqsanger.gz
	SRR8187000_2.fastq.gz	Fastqsanger.gz
	SRR8187010_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

Gene expression profiling of Î³34.5 deleted HSV1 infected Mouse Embryonic Fibroblasts

Project description:Gene expression analysis of wild type and STING knock-out Mouse Embryonic Fibroblasts (MEFs) infected with Î³34.5 deleted HSV1. Genes whose expression that are affected by HSV1 in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated. Primary MEFs were mock treated or infected with Î³34.5 deleted HSV1 at M.O.I. 1. Total RNA was extracted 3 hours post infection for array analysis.

2013-01-15 | E-GEOD-43479 | biostudies-arrayexpress

Gene expression profiling of γ34.5 deleted HSV1 infected Mouse Embryonic Fibroblasts

Project description:Gene expression analysis of wild type and STING knock-out Mouse Embryonic Fibroblasts (MEFs) infected with γ34.5 deleted HSV1. Genes whose expression that are affected by HSV1 in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated.

2013-01-15 | GSE43479 | GEO

mRNA-Sequencing data of herpes simplex virus type 1 (HSV1)-infected primary mouse microglia

Project description:We report mRNA-Sequencing analysis of primary mouse microglia infected with HSV1 and/or treated with ALT001, which is mitophagy inducing drug

2024-12-31 | GSE278015 | GEO

Cell-intrinsic Innate Immune Responses against Chikungunya Virus in a Human Ex Vivo Synovial Fibroblast Model

Project description:Purpose: Human primary synovial fibroblasts extracted from the knee were established as an ex vivo infection model for Chikungunya Virus. The cell-intrinsic immune response was determined using RNA-seq of infected and uninfected fibroblasts from healthy donors and donors with an osteoarthritic background. Methods: Fibroblasts of four osteoarthritic and two healthy donors were infected with CHIKV strain LR2006-OPY at an MOI of 10 in the presence or absence of the CHIKV neutralizing antibody C9 and total RNA was extracted at 24 hours post infection. Deep sequencing with paired-end reads was performed using an Illumina platform and data was analyzed with CLC Genomics Workbench 12 (QIAGEN) by mapping the human reads onto the hg19 reference genome scaffold (GCA_000001405.28). Unmapped reads not matching the human genome were subsequently mapped onto the CHIKV genome LR2006_OPY (DQ443544.2). Results: For osteoartritic fibroblasts ~25-35 Mio reads per sample, for healthy donor fibroblasts ~50-60 Mio reads per sample were achieved. Analysis revealed no major differences in the resting or infection-induced transcriptome (R2 = 0.9085 and 0.9086, respectively), yet some non-inflammation related pathways were significantly different regulated as determined by Gene Ontology analysis. Conclusion: Osteoarthritic fibroblasts were found to be an accessible source of primary cells suitable for studying CHIKV infection and pathophysiology. The cells did not majorly differ from the rarely avaiblabe healthy donor fibroblasts on the transcriptomic level, and did not show signs of pre-activation or inflammation in the absence of infection.

2020-06-19 | GSE152782 | GEO

Encephalitis and poor neuronal death-mediated control of herpes simplex virus in human inherited RIPK3 deficiency

Project description:We hypothesize that human RIPK3 deficiency does not result in impairment of type I IFN mediated antiviral immunity, contrasting with the situation in deficiencies of the TLR3-IFNAR1 circuit. To test the cellular responses to HSV1 at the wide transcriptome level, bulk RNA sequencing was performed with human primary fibroblasts without or with HSV-1 infection for 24 hours, in cells from healthy controls, RIPK3 HSE patient and other patients with recessive TLR3, IFNAR1 or NEMO deficiency.

2023-03-29 | GSE228495 | GEO

Targeted RNA sequencing of varicella zoster virus-infected human brain vascular adventitial fibroblasts

Project description:Transcriptome analysis of VZV infected primary human brain vascular adventitial fibroblasts (HBVAFs)

2021-11-17 | GSE175797 | GEO

Expression data from primary human dermal fibroblasts with STAT2 deficiency and control fibroblasts treated with interferon

Project description:Primary human dermal fibroblasts were isolated from an individual showing a genetic defect in innate antiviral immunity associated with profound failure of type 1 interferon signaling and absence of the STAT2 protein. The transcriptional response of these cells to a 10h treatment with interferon-alpha was compared with that of control dermal fibroblasts. We used microarrays to detail the global program of gene expression resulting from interferon-alpha treatment in STAT 2 deficient and control fibroblasts. Primary human dermal fibroblasts were grown in the presence or absence of 1,000U/ml interferon-alpha (IFNa) for 10 hours before RNA extraction and hybridization on Affymetrix microarrays.

2013-03-05 | E-GEOD-41960 | biostudies-arrayexpress

Mus musculus

Project description:Gene expression profiling of γ34.5 deleted HSV1 infected Mouse Embryonic Fibroblasts

| PRJNA186542 | ENA

RNA seq analysis of primary human macrophages exposed to atheroma plaques homogenates with or without the Liver X receptor (LXR) antagonist GSK 2033

Project description:To identify potential LXR target genes induced in the context of atherosclerosis we performed a transcriptomic analysis of human macrophages exposed or not to human carotid plaque homogenates in the presence or the absence of the LXR antagonist GSK 2033. We used primary macrophages from three distincts donors exposed to three differents plaque homogenates.

2020-05-19 | GSE125126 | GEO