Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144151 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mouse RAW264.7 macrophages were treated with LPS, IFNb, poly(rI:rC), poly(dA:dT), VSV, HSV, Sendai virus. Genes identified by Human Innate Immunity Interactome for type I Interferon (HI5) were examined for expression. qPCR gene expression profiling. RAW264.7 macrophages were used and treated separately as indicated in the summary. Equal amount total RNA from each group was used for gene expression analysis.
2011-09-08 | E-GEOD-31790 | biostudies-arrayexpress
Project description:We previously identified Tbc1d23 as a candidate novel regulator of innate immunity using comparative genomics RNAi screens in C. elegans and mouse macrophages. Using mice with an engineered knockout mutation in Tbc1d23 and macrophages engineered to overexpress Tbc1d23, we now show that Tbc1d23 is a general but not universal inhibitor of the innate immune response, inhibiting multiple Toll-like receptor (TLR) and Dectin signaling pathways but not NOD signaling pathways. Tbc1d23 likely acts downstream of the TLR signaling adaptors MyD88 and Trif and upstream of the transcription factor XBP1. Importantly, like XBP1, Tbc1d23 affects the maintenance but not initiation of inflammatory cytokine production induced by lipopolysaccharide (LPS). The identification of a novel temporal regulator of innate immunity signaling validates the comparative genomics approach for innate immunity gene discovery. Total of 24 samples; Tbc1d23-overexpressing line and control line; 0, 1, 3, and 5 hour LPS treatment; 3 biological replicates per group
2012-04-03 | E-GEOD-30840 | biostudies-arrayexpress
Project description:Setd1bKO primary murine bone marrow-derived macrophages (BMDMs) were treated with lipopolysaccharide (LPS) or dexamethasone and LPS (Dex+LPS) and gene expression differences in response to treatment analysed by PolyA RNA-Sequencing. No Dex-treatment dependent gene expression differences were identified. Setd1aDel/+ Raw264.7 cells with reduced Setd1a expression were analyzed with regards to their reponse to Dex when inflammatorily challenged with LPS by mRNA-Seq. We observed reduced GR-dependent gene acivation in Setd1a hypermorphic Raw264.7 cells. Wild type and Setd1aDel/+ Raw264.7 cells were treated with LPS or LPS and interferon beta (IFNB1) to show the IFNB1-dependent loss of gene expression in LPS-stimulated Setd1aDel/+ cells.
2020-12-31 | GSE137944 | GEO
Project description:Despite increasing evidence to indicate that long non-coding RNAs (lncRNAs) are novel regulators of immunity, there has been no systematic attempt to identify and characterise the lncRNAs whose expression are changed following the induction of the innate immune response. To address this issue, we have employed next generation sequencing data to determine the changes in the lncRNA profile in LPS-stimulated human macrophages, IL1beta-stimulated human airway A549 epithelial cells and and LPS-stimulated mouse RAW 264.7 macrophages
2017-10-01 | GSE101868 | GEO
Project description:Gene Expression Profiles of RAW264.7 Macrophages Stimulated with Two Commonly Used Preparations of LPS
| PRJNA126215 | ENA
Project description:EVs derived from lipopolysaccharide （LPS）-stimulated cardiomyocytes （EVLPS） exhibit anti-inflammatory effects on macrophages and reduce cardiac inflammation in mice.To investigate gene expression changes induced by EVLPS treatment in inflammatory RAW264.7 using next-generation sequencing，we performed RNAseq.
2024-10-23 | GSE279575 | GEO
Project description:Defective autophagy is linked to proinflammatory diseases. However, the mechanisms by which autophagy limits inflammation remain elusive. Here, we found that the pan-FGFR inhibitor LY2874455 efficiently activated autophagy and suppressed innate inflammation in macrophages stimulated by lipopolysaccharide (LPS). The mass spectrometry-based proteomics analysis of RAW264.7 cells treated with LPS (20ng/ml) and LY2874455 was performed. The protein levels of macrophages were systematically analyzed and quantified. Then, the protein levels were compared. The fold change and significance were analyzed. Multiplex proteomic profiling identified the immunoproteasome, a specific isoform of the 20s constitutive proteasome, as substrates that are degraded by selective autophagy. SQSTM1/p62 was found to be a selective autophagy-related receptor that mediated this degradation. Autophagy deficiency or p62 knockdown blocked the effects of LY2874455, leading to the accumulation of immunoproteasomes and increases in inflammatory reactions.
2024-05-24 | PXD038747 | Pride
Project description:Macrophages play a critical role in innate immunity, and the expression of early response genes orchestrate much of the initial response of the immune system. Macrophages undergo extensive transcriptional reprogramming in response to inflammatory stimuli such as Lipopolysaccharide (LPS). To identify gene transcription regulation patterns involved in early innate immune responses, we used two genome-wide approaches - gene expression profiling and chromatin immunoprecipitation-sequencing (ChIP-seq) analysis. We examined the effect of 2 hrs LPS stimulation on early gene expression and its relation to chromatin remodeling (H3 acetylation; H3Ac) and promoter binding of Sp1 and RNA polymerase II phosphorylated at serine 5 (S5P RNAPII), which is a marker for transcriptional initiation. Our results indicate novel and alternative gene regulatory mechanisms for certain proinflammatory genes. We identified two groups of up-regulated inflammatory genes with respect to chromatin modification and promoter features. One group, including highly up-regulated genes such as tumor necrosis factor (TNF), was characterized by H3Ac, high CpG content and lack of TATA boxes. The second group, containing inflammatory mediators (interleukins and CCL chemokines), was up-regulated upon LPS stimulation despite lacking H3Ac in their annotated promoters, which were low in CpG content but did contain TATA boxes. Genome-wide analysis showed that few H3Ac peaks were unique to either +/-LPS condition. However, within these, an unpacking/expansion of already existing H3Ac peaks was observed upon LPS stimulation. In contrast, a significant proportion of S5P RNAPII peaks (approx 40%) was unique to either condition. Furthermore, data indicated a large portion of previously unannotated TSSs, particularly in LPS-stimulated macrophages, where only 28% of unique S5P RNAPII peaks overlap annotated promoters. The regulation of the inflammatory response appears to occur in a very specific manner at the chromatin level for specific genes and this study highlights the level of fine-tuning that occurs in the immune response. 4 pairs of THP-1 cells either stimulated with LPS or not This submission represents transcriptome component of study.
2012-03-07 | E-GEOD-32141 | biostudies-arrayexpress
Project description:Macrophages play a critical role in innate immunity, and the expression of early response genes orchestrate much of the initial response of the immune system. Macrophages undergo extensive transcriptional reprogramming in response to inflammatory stimuli such as Lipopolysaccharide (LPS). To identify gene transcription regulation patterns involved in early innate immune responses, we used two genome-wide approaches - gene expression profiling and chromatin immunoprecipitation-sequencing (ChIP-seq) analysis. We examined the effect of 2 hrs LPS stimulation on early gene expression and its relation to chromatin remodeling (H3 acetylation; H3Ac) and promoter binding of Sp1 and RNA polymerase II phosphorylated at serine 5 (S5P RNAPII), which is a marker for transcriptional initiation. Our results indicate novel and alternative gene regulatory mechanisms for certain proinflammatory genes. We identified two groups of up-regulated inflammatory genes with respect to chromatin modification and promoter features. One group, including highly up-regulated genes such as tumor necrosis factor (TNF), was characterized by H3Ac, high CpG content and lack of TATA boxes. The second group, containing inflammatory mediators (interleukins and CCL chemokines), was up-regulated upon LPS stimulation despite lacking H3Ac in their annotated promoters, which were low in CpG content but did contain TATA boxes. Genome-wide analysis showed that few H3Ac peaks were unique to either +/-LPS condition. However, within these, an unpacking/expansion of already existing H3Ac peaks was observed upon LPS stimulation. In contrast, a significant proportion of S5P RNAPII peaks (approx 40%) was unique to either condition. Furthermore, data indicated a large portion of previously unannotated TSSs, particularly in LPS-stimulated macrophages, where only 28% of unique S5P RNAPII peaks overlap annotated promoters. The regulation of the inflammatory response appears to occur in a very specific manner at the chromatin level for specific genes and this study highlights the level of fine-tuning that occurs in the immune response. 2 pairs of THP-1 cells either stimulated with LPS or not. ChIP using either H3K9/K14Ac, RNA Pol II (phospho S5) or SP1 antibody. This submission represents chip-seq component of study.
2012-03-07 | E-GEOD-32324 | biostudies-arrayexpress
Project description:Lipopolysaccharide (LPS)/immunue complex (IC) stimulated macrophages produce cytokine profiles that differe from LPS-stimulated inflammatory macropahges. Notch signaling is activated in LPS/IC-stimulated macrophages and inhibition of Notch signaling reduced IL-10 production. This study investigated the effect of gamma-secretase inhibitor (GSI) that suppresses Notch signaling pathway, on gene expression profiles in macrophages activated by LPS/IC.
2018-06-21 | GSE114020 | GEO