Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of genes regulated by Akirin and Brahma upon IMD pathway activation in drosophila S2 cells

ABSTRACT: This micro-array helps establishing the function of Akirin, a nuclear protein with unknown domains, a putative interacting partner, in the transcriptional regulation of the targets of Relish, a NF-kB factor required to fight Gram(-) bacteria infection in Drosophila melanogaster.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE54915 | GEO | 2014/11/05

SECONDARY ACCESSION(S): PRJNA238018

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Analysis of genes regulated by Akirin and Brahma upon IMD pathway activation in drosophila S2 cells

Project description:This micro-array helps establishing the function of Akirin, a nuclear protein with unknown domains, a putative interacting partner, in the transcriptional regulation of the targets of Relish, a NF-kB factor required to fight Gram(-) bacteria infection in Drosophila melanogaster. S2 cells were knocked down for Relish, Akirin and immune-challenged by Calcium-phosphate transient transfection of dsRNA and over-expressing PGRP-LC vector. Positively transfected cells were sorted by co-expressed Tomato and RNA was purified and analysed by a micro-array

2014-11-05 | E-GEOD-54915 | biostudies-arrayexpress

Transcriptome study of colon epithelial cells in Reg3a-transgenic mice

Project description:The human C-type lectin Reg3a (HIP/PAP) is an antimicrobial peptide that kills Gram-positive bacteria. Reg3a preserves gut microbiota homeostasis, reinforces intestinal barrier function and thereby helps to fight induced colitis in mice. Transcriptomic data revealed an upregulation of numerous genes involved in the robustness of the intestinal barrier, and the biosynthesis pathway of mucin core 1 and 3 O-glycans.

2018-01-31 | GSE64932 | GEO

RNAi knock down of Imd, Basket and Relish in Drosophila cells treated with LPS and luciferase

Project description:Imd, Basket and Relish (the Drosophila JNK and NF-kB homolog, respectively) genes were knock-downed individually by RNAi, and we compared the gene expression patterns in response to LPS with those of control samples treated with luciferase RNAi.

2004-10-01 | E-MEXP-177 | biostudies-arrayexpress

Relish-mediated lncRNA-CR33942 facilitates Drosophila Imd immune responses and promotes antimicrobial peptide expression via interacting with Relish

Project description:Long noncoding RNAs (lncRNAs), as a class of emerging regulators, play crucial role in regulating the strength and duration of innate immunity. However, little is known about how these Drosophila Imd immunity-related lncRNAs are regulated. Herein, we firstly revealed that overexpression of lncRNA-CR33942 could strengthen the expression of Imd pathway antimicrobial peptides Diptericin (Dpt) and Attacin-A (AttA) after infection, and vice versa. Secondly, RNA-seq analysis of post-infected lncRNA-CR33942-overexpressing flies further confirmed that lncRNA-CR33942 positively regulates the Drosophila Imd pathway. Mechanistically, we indicated that lncRNA-CR33942 interacts with NF-κB transcription factor Relish to promote its binding to Dpt and AttA promoters, thereby facilitating Dpt and AttA expression. Interestingly, we found that Relish can also directly promote lncRNA-CR33942 transcription by binding to its promoter. Finally, rescue experiments and dynamic expression profiling post-infection demonstrated the vital role of the Relish/lncRNA-CR33942/AMPs regulatory axis in enhancing inadequate Imd immune responses and maintaining immune homeostasis. Taken together, our study not only elucidates a novel mechanism about lncRNA in Drosophila Imd immune regulation, but also has important guiding significance for elucidating the complex regulatory mechanism of animal innate immune response.

2022-03-22 | GSE198991 | GEO

Relish-mediated lncRNA-CR33942 facilitates Drosophila Imd immune responses and promotes antimicrobial peptide expression via interacting with Relish

Project description:Relish-mediated lncRNA-CR33942 facilitates Drosophila Imd immune responses and promotes antimicrobial peptide expression via interacting with Relish

| PRJNA817795 | ENA

Analysis of genes regulated by miRNAs upon Toll pathway activation in shmCherry and shAgo1 flies

Project description:This micro-array helps establish Toll activated-genes dampened by miRNAs in Drosophila melanogaster.

2024-06-05 | GSE133877 | GEO

The effect of osa RNAi with and without infection

Project description:Transcriptome profiling of immune-responsive genes in Drosophila melanogaster during Gram-positive bacterial infection and upon silencing of osa was performed. The most highly induced gene in the control set (150071 Valanne I) by Micrococcus luteus infection was CR44404, and its expression is fully dependent on osa expression (as shown in this dataset, 150071 Valanne II). The full transcriptome analysis also indicated that Osa regulates the expression of immune genes by modifying the expression of the Drosophila NF-kappaB factors Relish and Dif.

2020-02-13 | GSE120443 | GEO

Loss of self-tolerance leads to altered gene expression and IMD pathway activation in Drosophila melanogaster

Project description:Immune self-tolerance is the ability of a host’s immune system to recognize and avoid triggering immune responses against self-tissue. This allows the host to avoid self-directed immune damage, while still responding appropriately to pathogen infection. A breakdown of self-tolerance can lead to an autoimmune state in which immune cells target healthy self-tissue, leading to inflammation and tissue damage. In order to better understand the basic biology of autoimmunity and the role of the innate immune system in maintaining self-tolerance, we have recently characterized the Drosophila melanogaster tuSz autoimmune mutant. This mutant strain can serve as a model of innate immune mediated self-tolerance, and here we identify transcripts that are deregulated in flies experiencing a loss of self-tolerance. We found that these changes include the ectopic activation of pro-inflammatory signaling through the Relish/NFκB transcription factor, alterations in transcripts encoding proteins predicted to mediate organismal metabolism, and a downregulation of transcripts linked to developmental processes. This study can provide insight into the transcriptional and physiological changes underlying self-tolerance and autoimmunity.

2024-11-12 | GSE189383 | GEO

Drosophila Schneider S2 cell TFIIA-L Immunoprecipitation

Project description:In order to identify interaction partner of the Drosophila melanogaster TFIIA protein, we have immunoprecipitated an endogenously 3xFLAG-AID tagged TFIIA-L from Drosophila Schneider S2 cells

2023-02-16 | PXD028094 | Pride

Proinflammatory stimuli engage Brahma related gene 1 and Brahma in endothelial injury.

Project description:Endothelial dysfunction inflicted by inflammation is found in a host of cardiovascular pathologies. One hallmark event in this process is the aggregation and adhesion of leukocyte to the vessel wall mediated by the upregulation of adhesion molecules (CAM) in endothelial cells at the transcriptional level. The epigenetic modulator(s) of CAM transactivation and its underlying pathophysiological relevance remain poorly defined.Our goal was to determine the involvement of Brahma related gene 1 (Brg1) and Brahma (Brm) in CAM transactivation and its relevance in the pathogenesis of atherosclerosis.In the present study, we report that proinflammatory stimuli augmented the expression of Brg1 and Brm in vitro in cultured endothelial cells and in vivo in arteries isolated from rodents. Overexpression of Brg1 and Brm promoted while knockdown of Brg1 and Brm abrogated transactivation of adhesion molecules and leukocyte adhesion induced by inflammatory signals. Brg1 and Brm interacted with and were recruited to the CAM promoters by nuclear factor ?B/p65. Conversely, depletion of Brg1 and Brm disrupted the kinetics of p65 binding on CAM promoters and crippled CAM activation. Silencing of Brg1 and Brm also altered key epigenetic changes associated with CAM transactivation. Of intrigue, 17?-estradiol antagonized both the expression and activity of Brg1/Brm. Most importantly, endothelial-targeted elimination of Brg1/Brm conferred atheroprotective effects to Apoe(-/-) mice on a Western diet.Our data suggest that Brg1 and Brm integrate various proinflammatory cues into CAM transactivation and endothelial malfunction and, as such, may serve as potential therapeutic targets in treating inflammation-related cardiovascular diseases.

| S-EPMC4049295 | biostudies-literature

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