Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

ABSTRACT: Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

PROVIDER: PRJNA733905 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14692802_1.fastq.gz	Fastqsanger.gz
	SRR14692802_2.fastq.gz	Fastqsanger.gz
	SRR14692803_1.fastq.gz	Fastqsanger.gz
	SRR14692803_2.fastq.gz	Fastqsanger.gz
	SRR14692804_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

Project description:Upon tick borne encephalitis virus exposure of brain-resident cells, astrocytes are important IFN-β producers that followed a biphasic response, which initially depends on MAVS- and later on MyD88/TRIF-signaling

2021-09-28 | GSE175823 | GEO

Myd88, Trif, and Rip2-independent macrophage responses to Legionella pneumophila

Project description:Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila. Keywords: Expression profiling by microarray

2008-11-15 | GSE13147 | GEO

Transcription profiling of mouse Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophages after infection with wild type or dotA mutant L. pneumophila

Project description:Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila. Experiment Overall Design: Bone marrow-derived macrophages from Myd88-/-Trif-/- and Myd88-/-Rip2-/- mice were infected with WT L. pneumophila (Lp02) or dotA mutant L. pneumophila (Lp03) for 4 hours. The RNA was extracted, processed, and hybridized onto Affymetrix 430 2.0 microarrays

2008-11-22 | E-GEOD-13147 | biostudies-arrayexpress

Transcription profiling of mouse LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- animals

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14890 | biostudies-arrayexpress

Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice.

2009-02-19 | GSE14890 | GEO

Tick-borne encephalitis virus

Project description:Tick-borne encephalitis virus Raw sequence reads

| PRJNA1174237 | ENA

Tick-borne encephalitis virus

Project description:Tick-borne encephalitis virus Genome sequencing and assembly

| PRJNA953225 | ENA

Tick-borne encephalitis virus

Project description:Tick-borne encephalitis virus Genome sequencing and assembly

| PRJNA587877 | ENA

The effect of Monophosphoryl Lipid A (MPLA) on gene expression of wild type, MyD88 KO, and TRIF KO bone marrow-derived macrophages

Project description:We aimed to determine the relative contributions of MyD88- and TRIF-dependent signaling in Toll-like receptor-induced trained immunity in macrophages.

2022-10-28 | GSE205186 | GEO

In vitro responses of PBMC and fibroblasts from patients with TRIF deficiency after TRIF dependent and independent stimuli

Project description:We report here unrelated HSE patients with autosomal recessive (AR) or autosomal dominant (AD) TRIF deficiency. The AR form of the disease is due to a homozygous nonsense mutation, resulting in a complete absence of the TRIF protein. Both the TLR3 and the TRIF-dependent TLR4 signaling pathways are abolished. The AD form of TRIF deficiency is due to a heterozygous missense mutation resulting in a dysfunctional protein. The TLR3 signaling pathway is impaired, whereas the TRIF-dependent TLR4 pathway is unaffected. Both patients however showed reduced capacity to respond to cytosolic double stranded RNA, consistent with recent reports of TRIF’s involvement in the DExD/H-box helicases pathway. Skin fibroblast cell lines were derived from healthy controls (n=3), patient with deficiencies for TRIF (n=1), MYD88 (n=1), and TLR3 (n=1) and cultured for 4 hours in the presence of IL1B (20ng/ml) or poly I:C (25ng/ml) or left unstimulated for the same length of time. PBMCs (previously frozen) collected from a healthy control (n=1) and patients with deficiencies for TRIF (n=1), and MYD88 (n=1) were cultured together with LPS (10ng/ml) or R848 (3ug/ml) for 2hrs or left unstimulated for the same length of time.

2011-10-19 | E-GEOD-32390 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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