Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA111959 | ENA |
REPOSITORIES: ENA
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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
Project description:MyD88-independent signal transduction associated with Toll-like receptors (TLRs) 3 and TLR4 is mediated through the adapter protein TRIF (TIR-domain-containing adapter-inducing interferon-beta). It has been proposed that TLR signalling is important for the transcription of crucial inflammasome components like NLRP3, a process that has been termed "priming". In order to test whether TRIF signalling was required for the priming of inflammasome components, we performed a genome wide transcriptional analysis on wild-type and Trif-knockout bone marrow derived macrophages (BMMs) before and 1, 3 and 6 hours after phagocytosis of E. coli. These results indicated that TRIF was involved in the activation and not transcriptional priming of the NLRP3 inflammasome. Bone marrow derived macrophages from WT and Trif knockout mice, stimulated with E.coli for up to 6hrs.
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Project description:Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice.
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Project description:Pre-stimulation of MDMs with LPS (signals via MyD88 and TRIF dependent pathways) and PolyI:C (signals via a TRIF dependent pathway) leads to a reduced viral infection. In contrast, pre-stimulation with P3C (signals via MyD88 dependent pathway) does not lead to a reduced viral infection. This microarray was performed to find genes that are specifically upregulated in LPS and PolyI:C stimulated MDMs but not P3C stimulated MDMs. So to give us leads into the mechanism involved in the reduction of viral infection.
2013-07-01 | GSE41295 | GEO
Project description:Pre-stimulation of MDMs with LPS (signals via MyD88 and TRIF dependent pathways) and PolyI:C (signals via a TRIF dependent pathway) leads to a reduced viral infection. In contrast, pre-stimulation with P3C (signals via MyD88 dependent pathway) does not lead to a reduced viral infection. This microarray was performed to find genes that are specifically upregulated in LPS and PolyI:C stimulated MDMs but not P3C stimulated MDMs. So to give us leads into the mechanism involved in the reduction of viral infection. MDMs of four different donors were stimulated for 4h with mock, LPS, PolyI:C or P3C. RNA was isolated and gene expression of these cells was assessed. Gene expression of LPS, PolyI:C and P3C stimulated MDMs was compared to mock.
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Project description:Expression data of LPS-stimulated macrophages in wild-type and LysM-Cre+ Akirin2fl/fl mice
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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
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Project description:Toll-like receptors (TLRs) are present on the membranes of immune cells such as dendritic cells, macrophages, and natural killer cells. It is essential for the recognition of microbiological components. They trigger both innate and adaptive immune responses against pathogenic microorganisms. Among TLRs, TLR4 is one of the well-studied receptors that recognizes lipopolysaccharide (LPS) and initiates the TRIF- and MyD88-dependent signaling cascades. Regulators in TLR4 signaling, including protein kinases, play a key role in innate and adaptive immune responses. Protein phosphorylation on serine, threonine, and tyrosine is essential regulatory post-translational modification (PTM) because it serves as a signal transduction mechanism enabling the cells to connect extracellular signals to the regulation of multiple biological processes. Although phosphoproteins in TLR4 signaling pathways have been extensively investigated by mass spectrometry using data-dependent acquisition (DDA), the phosphoproteins that initiate TLR4 signaling cascades remain poorly understood due to technical limitations. We utilized data-independent acquisition (DIA) to get comprehensive information on phosphorylation inside LPS-stimulated TLR4 signaling pathways in macrophages.
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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. Keywords: Time course after LPS (100 ng/ml) stimulation
2009-02-19 | GSE14890 | GEO
Project description:Toll-like receptor 4 (TLR4) plays a pivotal role in the host response to lipopolysaccharide (LPS), a major cell wall component of Gram-negative bacteria. Here we elucidated whether the endocytic adaptor protein Disabled-2 (Dab2) that is abundantly expressed in the macrophages plays a role in LPS-stimulated TLR4 signaling and trafficking. Molecular analysis and transcriptome profiling of the RAW264.7 macrophage-like cells expressing short-hairpin RNA of Dab2 revealed that Dab2 mainly regulated LPS-stimulated TRIF-dependent, but not MyD88-dependent TLR4 signaling. Consequently, knockdown of Dab2 augmented TRIF-dependent interferon regulatory factor 3 activation and the expression for the subsets of inflammatory cytokines and interferon-inducible genes. We further delineated that Dab2 acted as a “clathrin sponge” and sequestered clathrin from TLR4/MD2 complex in the resting stage of macrophages. Clathrin was released from Dab2 and associated with TLR4 to facilitate the internalization of TLR4/MD2 complex together with the bound ligand from the cell surface upon LPS stimulation. Dab2 thereby functions as a negative immune regulator of TLR4 endocytosis and signaling, supporting a novel role of Dab2-associated regulatory circuit in the control of inflammatory response of macrophage to endotoxin.
2017-02-09 | GSE81088 | GEO