Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin accessibility analysis of wild type bone marrow-derived macrophages in response to Anisomycin, type I interferons and the combination of them or with p38 MAPK inhibitor PH-797804 (ATAC-Seq IFNb)

ABSTRACT: The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show changes in chromatin accessibility upon Anisomycin, a drug that induces stress-activation of MAPK pathways, IFNb stimulation and the combination of both or with p38 inhibitor PH-797804, Anisomycin and IFNb.

ORGANISM(S): Mus musculus

PROVIDER: GSE199125 | GEO | 2022/12/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profile analysis of wild type bone marrow derived-macrophages in response to Anisomycin, type I and type II interferons and the combination of them

Project description:The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show how Anisomycin, a drug that induces stress-activation of MAPK pathways, regulates mRNA expression of interferon stimulated genes (ISG) upon IFNg and IFNb stimulation

2022-12-18 | GSE199128 | GEO

Chromatin accessibility analysis of wild type bone marrow-derived macrophages in response to Anisomycin, type II interferon and the combination of them or with p38 MAPK inhibitor PH-797804 (ATAC-Seq IFNg)

Project description:The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show changes in chromatin accessibility upon Anisomycin, a drug that induces stress-activation of MAPK pathways, IFNg stimulation and the combination of both or with p38 inhibitor PH-797804, Anisomycin and IFNg.

2022-12-18 | GSE199126 | GEO

c-Jun and CREB1 transcription factor binding analysis in wild type bone marrow-derived macrophages in response to type II interferon and stress

Project description:The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show c-Jun and CREB binding upon Anisomycin, a drug that induces stress-activation of MAPK pathways, IFNg stimulation and the combination of both or with p38 inhibitor PH-797804 and JNK inhibitor SP600125, Anisomycin and IFNg.

2022-12-18 | GSE199127 | GEO

Expression data from anisomycin- and imiquimod-induced dermatitis

Project description:We provide a new psoriasis mouse model which is induced by p38 activation in skin. We compared the individual transcriptomic proﬁles of anisomycin and imiquimod-induced dermatitis. We used microarrays to compare the gene expression pattern between anisomycin- and imiquimod- induced dermatitis.

2019-02-15 | GSE110658 | GEO

Genes in apoptosis induced by anisomycin in human leukemia U937 cells

Project description:Anisomycin is known as a potent apoptosis inducer by activating JNK/SAPK and inhibiting protein synthesis during translation. However, only few details are known on the mechanism of apoptosis induced by this compound. Genes in apoptosis induced by anisomycin in human leukemia U937 cells were investigated by using an Affymetrix GeneChip system. DNA fragmentation and phosphatidylserine externalization assays clearly demonstrated that anisomycin induced apoptosis in a time- and concentration- dependent manner. Of 22,283 probe sets analyzed, this compound down-regulated 524 probe sets and up-regulated 523 by a factor 1.5 or greater. Keywords: anisomycin, gene expression, Human lymphoma U937 cell

2007-06-23 | GSE8229 | GEO

Pharmacogenomics of IFNb therapy

Project description:This experiment set is used for the manuscript entitled: Pharmacogenomics of Interferon-b therapy in multiple sclerosis: Baseline IFN signature determines pharmacological differences between patients. In this study we generated and analyzed pre- and post- IFNb treatment gene expression patterns of RRMS patients with the aim of identifying pre-existing and/or drug-induced signatures that will allow us to make predictions on the expected pharmacological effects of IFNb treatment. We show that the expression level of IFN response genes prior to treatment, determines the pharmacological differences between patients with MS at the molecular level. A group of 16 Dutch patients (10 females and 6 males) with clinically definite relapsing-remitting MS was recruited from the outpatient clinic of the MS Centre Amsterdam. Mean age at start of IFNb therapy is 40.6 +/- 7.7, mean EDSS is 2.3 +/- 1.3 (range 1-6). Blood samples were obtained just before treatment and 1 month after start of the therapy. Patients received Avonex, Betaferon, Rebif 22 or Rebif 44. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Before and 1 month after IFNb therapy Keywords: compound_treatment_design Complex

2008-04-01 | E-GEOD-10655 | biostudies-arrayexpress

Pharmacogenomics of IFNb therapy

2008-04-01 | GSE10655 | GEO

Impact of MEM40 and IFNB on human DC activation markers

Project description:To determine the impact of MEM40 and IFNB on normal human donor monocyte-derived DCs (Mo-DCs) phenotype, we used an experimental design where human A549 lung cancer cells were first infected with Ad-Null or adenoviruses expressing human IFNB, MEM40 or MEM40 + IFNB, followed by removal of virus-containing supernatant and co-culture with Mo-DCs. We used the above design followed by sorting of MHC-II+ CD11c+ cells for bulk RNA-sequencing.

2023-02-13 | GSE223342 | GEO

Gene-profile comparison of wt and Ifnb–/– cerebellar granular neurons

Project description:Interferon-b (IFN-b) belongs to the type I interferon family of cytokines and via binding to its receptor, interferon-a/b-receptor (IFNAR), it exerts immunoregulatory effects such as anti-viral and anti-inflammatory properties, and clinical benefits for patients with the CNS disease multiple sclerosis. To compare differentially regulated genes in neurons of interferon-beta knock out mice (Ifnb–/–), we conducted a microarray analysis on cerebellar granular neurons (CGNs) from wt (Ifnb+/+) and Ifnb-/- mice with or without treatment with recombinant IFN-b.

2015-10-08 | GSE63815 | GEO

LPS-induced IFN networks predict severe viral Lower Respiratory tract Infections in infancy

Project description:Severe LRIs are a major cause of infant/child hospitalization and a risk factors for asthma pathogenisis. Innate immune interactions with microbial pathogens, esp. in early life, underpin risk. We aimed to characterize cord blood mononuclear cell (CBMC) responses to activation of micriobial recognition receptors (TLRs 3, 4, & 7) and identify response pattern variations associated withsLRI susceptibility in infancy.

2022-08-24 | GSE184383 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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