Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deficiency of RPSA reduces binding of P65 to proinflammatory cytokines promoter regions in HSV-1 infection

ABSTRACT: After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

ORGANISM(S): Mus musculus

PROVIDER: GSE204891 | GEO | 2023/11/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Deficiency of Rpsa results in reduced levels of H3K4me3 in inflammatory cytokines promoter regions

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the level of H3K4me3 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204890 | GEO

Ribosome protein RPSA promotes the expression of proinflammatory cytokines induced by HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA. To further verify the biological function of RPSA, we constructed the RPSA-deficient RAW264.7 macrophage cell line with the inducible CRISPR-Cas9 system, then found that the deletion of RPSA could effectively reduce the expression of proinflammatory cytokines such as IL-1α, IL-1β, IL-6, IL-12 and TNFα induced by HSV-1 infection.

2023-11-12 | GSE204893 | GEO

ATAC-seq analysis in Rpsa-iKO RAW264.7 cells after HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ATAC-seq, we found that chromatin accessibility around transcription start sites (TSS) of proinflammatory cytokinse in HSV-1 infected Rpsa-iKO RAW264.7 was significantly reduced

2023-11-12 | GSE204889 | GEO

RPSA and proinflammatory cytokines after HSV-1 infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-12 | GSE204895 | GEO

IFN-λ signaling protects mice from severe HSV-1 skin disease II

Project description:Type III interferons (IFN-λ) are antiviral and immunomodulatory cytokines that have been best characterized in respiratory and gastrointestinal infections, but the effects of IFN-λ against skin infections have not been extensively investigated. We sought to define the skin-specific effects of IFN-λ against the highly prevalent human pathogen herpes simplex virus (HSV). We infected mice lacking the IFN-λ receptor (Ifnlr1-/-), both the IFN-λ and the IFN-αβ receptor (Ifnar1-/- Ifnlr1-/-), or IFN-λ cytokines (Ifnl2/3-/-) and found that IFN-λ restricts the severity of HSV-1 and HSV-2 skin lesions, independent of a direct effect on viral load. Using conditional knockout mice, we found that IFN-λ signaling in both keratinocytes and neutrophils was necessary to control HSV-1 skin lesion severity, and that IFN-λ signaling in keratinocytes suppressed CXCL9-mediated neutrophil recruitment to the skin. Furthermore, depleting neutrophils prevented the development of severe HSV-1 skin lesions in Ifnlr1-/- mice. Altogether, our results suggest that IFN-λ plays an immunomodulatory role in the skin that restricts neutrophil-mediated pathology during HSV infection, and suggest potential applications for IFN-λ in treating viral skin infections.

2023-09-12 | GSE242170 | GEO

IFN-λ signaling protects mice from severe HSV-1 skin disease I

2023-09-12 | GSE242068 | GEO

Transcriptional change of THP-1 after HSV-1UL37WT or HSV-1UL37C819S

Project description:we reporter the transcritional difference after THP-1 cells were infected with HSV-1UL37WT virus or HSV-1UL37C819S virus.

2018-05-29 | GSE114966 | GEO

IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

Project description:IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

| PRJNA416508 | ENA

Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

Project description:Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

| PRJNA656998 | ENA

Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs. Agilent Custom Chicken Gene Expression 8X60k (AMADID: G4102A_059389) designed by Genotypic Technology Private Limited , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)

2016-07-04 | E-GEOD-65231 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data