Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263418 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1611130_1.fastq.gz | Fastqsanger.gz | |||
| SRR1611130_2.fastq.gz | Fastqsanger.gz | |||
| SRR1611560_1.fastq.gz | Fastqsanger.gz | |||
| SRR1611560_2.fastq.gz | Fastqsanger.gz | |||
| SRR1611561_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 33 |
Similar Datasets
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:We report the application of bulk RNA sequencing for profiling changes in mouse cardiac lysates as a result of changes in innate immunity function. We generated an inducible endothelial cell toll-like receptor 2 knockout and assessed changes in overall gene expression in the absence of pathogen presence. We find that over 200 genes are differentially regulated between the two genotypes that are solely due to the presence of endogenous signaling within these animals. We also show that the genes that are differentially regulated are tied to the immunity function of the endothelium and that removal of toll-like receptor 2 signaling creates a diminished response by the immune system to wound healing and tumor development. Finally, we demonstrate that other immunomodulatory pathways are further affected, suggesting that changes outside of the endothelium are driven by endothelial-toll-like receptor 2 signaling. This study provides a framework for the application of tissue specific knockouts and profiling the role of endothelial as an innate immunity organ.
2021-05-19 | GSE155090 | GEO
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.
2012-04-04 | GSE30840 | GEO
Project description:Innate immunity in Drosophila acts as an organismal surveillance system that measures external stimuli or cellular fitness and triggers context-specific responses to fight infections and maintain tissue homeostasis. However, uncontrolled activation of innate immune pathways can be detrimental to the system. In mammals, innate immune signaling is often overactivated in malignant cells and contributes to tumor progression. Drosophila tumor models have been instrumental in the discovery of interactions between pathways that promote tumorigenesis, but little is known about whether and how the Toll innate immune pathway interacts with oncogenes. Here we use a Drosophila epithelial in vivo model to investigate the interplay between Toll signaling and oncogenic Ras.
2024-10-29 | GSE266879 | GEO
Project description:The project is oriented to study the infectivity of small ruminant lentiviruses (SRLVs) to epithelial cells in milk of goats and to analysis of genes encoding Toll-like receptor (TLR) on blood leukocytes of SRLV-infected goats with different levels of infection. The results will provide data on innate immunity in the course of SRLV infection.
2021-01-04 | PRJEB42246 | EVA
Project description:Salmonella causes inflammation in infected hosts. Inflammation is a well-characterized defensive mechanism of innate immunity. The recognition and engagement of lipopolysaccharide (LPS) endotoxins in the outer membranes of Salmonella to Toll-like receptor 4 of immune cells (macrophages and dendritic cells) trigger inflammatory responses characterized by secretion of pro-inflammatory cytokines, including TNF-beta, IL-1 and IL-6. These cytokines cause fever, anorexia, bodyweight losses, and catabolism of skeletal muscles and adipose tissues. However, molecular events underlying innate immune responses and metabolic activities during the later stage of inflammation are poorly understood. Additionally, the effects of prebiotics and antibiotics on innate immunity and nutrient metabolism are not yet reported. The objective of this study is to investigate the effects of a mannanoligosaccharide (MOS) prebiotic and virginiamycin (VIRG) sub-therapeutic antibiotic on innate immunity and glucose metabolism during late inflammation. We induced Salmonella LPS-systemic inflammation in a chicken model. Differentially regulated gene expressions were measured using 2 colour focussed oligonucleotide chicken-specific microarrays. Microarray analysis was performed on liver, intestinal and skeletal muscle tissues. We found that late inflammation was principally modulated by interleukin 3 (IL 3) and that glucose was mobilized from gluconeogenesis occurring in the intestines only. MOS and VIRG modulated innate immunity and metabolic genes differently. In contrast to VIRG, MOS terminated inflammatory responses earlier. Our results indicate IL 3 gene up-regulation in VIRG-fed chickens. To meet the higher energy requirements of VIRG chickens, genes for intestinal gluconeogenesis and liver glycolysis were respectively induced. Our study reveals the potential mechanisms by which prebiotic and antibiotic modulated innate immunity and glucose metabolism during late inflammation. 14-day old chickens were injected i.p. with saline or LPS. For each tissue and experimental conditions (saline or LPS challenge), a total of 12 microarrays (6 MOS birds + 6 VIRG birds) were used in a 2 x 2 factorial design and complete interwoven loop arrangement. We compared gene expression from prebiotic-fed birds with antibiotic-fed birds without including reference RNA. LPS challenge, antibiotic or prebiotic, innate immunity, glucose metabolism
2011-04-30 | E-GEOD-28959 | biostudies-arrayexpress
Project description:The innate immune system is the organism’s first line of defense against pathogens. Pattern recognition receptors (PRRs) are responsible for sensing the presence of pathogen-associated molecules. The prototypic PRRs, the membrane-bound receptors of the Toll-like receptor (TLR) family, recognize pathogen-associated molecular patterns (PAMPs) and initiate an innate immune response through signaling pathways that depend on the adaptor molecules MyD88 and TRIF. Deciphering the differences in the complex signaling events that lead to pathogen recognition and initiation of the correct response remains challenging. Here we report the discovery of temporal changes in the protein signaling components involved in innate immunity. Using an integrated strategy combining unbiased proteomics, transcriptomics and macrophage stimulations with three different PAMPs, we identified differences in signaling between individual TLRs and revealed specifics of pathway regulation at the protein level.
2017-06-12 | GSE85448 | GEO
Project description:The innate immune system is the organism’s first line of defense against pathogens. Pattern recognition receptors (PRRs) are responsible for sensing the presence of pathogen-associated molecules. The prototypic PRRs, the membrane-bound receptors of the Toll-like receptor (TLR) family, recognize pathogen-associated molecular patterns (PAMPs) and initiate an innate immune response through signaling pathways that depend on the adaptor molecules MyD88 and TRIF. Deciphering the differences in the complex signaling events that lead to pathogen recognition and initiation of the correct response remains challenging. Here we report the discovery of temporal changes in the protein signaling components involved in innate immunity. Using an integrated strategy combining unbiased proteomics, transcriptomics and macrophage stimulations with three different PAMPs, we identified differences in signaling between individual TLRs and revealed specifics of pathway regulation at the protein level. In addition to forming macrophages and dendritic cells, monocytes in adult peripheral blood retain the ability to develop into osteoclasts, mature bone-resorbing cells. The extensive morphological and functional transformations that occur during osteoclast differentiation require substantial reprogramming of gene and protein expression. Here we employ -omic-scale technologies to examine in detail the molecular changes at discrete developmental stages in this process (precursor cells, intermediate osteoclasts, and multinuclear osteoclasts), quantitatively comparing their transcriptomes and proteomes.
2016-10-12 | GSE87805 | GEO
Project description:we cloned and overexpressed human TTP-encoding gene ZFP36 in HeLa cell in the absence of inflammatory stimuli. The transcriptomes of the control and ZFP36-overexpression cells were sequenced and subjected to analysis and validation. Upon ZFP36 overexpression, expression of genes in innate immunity, including those in type I interferon signaling pathway and viral response, were specifically up-regulated, implying a transcriptional regulatory mechanism associated with the predicted DNA binding activity of TTP. TTP preferentially regulates the alternative splicing of genes involved in positive regulation of I-B/NF-B cascade and TRIF-dependent toll-like receptor signaling pathway, MAPK signaling pathway, TNF signaling pathway and T cell receptor signaling pathways.Our study indicates that TTP may regulates immune response via alternative splicing regulation and possibly by transcriptional regulation as well, which greatly expands the current understanding of the central role of TTP in regulating immune response and tumorigenesis.
2019-03-24 | GSE114216 | GEO
Project description:Innate immune responses of plant cells confer the first line of defence against pathogens. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. The Arabidopsis Toll-related intracellular receptor RPS4 operates inside nuclei to trigger resistance and defence gene reprogramming through the stress response regulator, EDS1. In order to test a role for RPS4 at the chromatin level during Effector-Triggered Immunity (ETI), we undertook a ChIP-seq approach.
2017-09-02 | GSE40329 | GEO