Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

15 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

ABSTRACT: DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages. Two independent bone marrow-derived macrophage cultures for each genotype (LysMcre/+ and Scid: Atmc/c: LysMcre/+) were infected with Listeria monocytogenes for 24 hrs at an MOI of 5. RNA was isolated using RNeasy (Qiagen). Gene expression profiling was performed using Illumina MouseRef-8 expression microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Barry Sleckman

PROVIDER: E-GEOD-70467 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

Project description:DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages.

2015-07-03 | GSE70467 | GEO

Intracellular transcription by multiple Listeria monocytogenes strains

Project description:These studies were designed to examine the transcription of Listeria monocytogenes strains 10403S and LO28 during intracellular replication in mammalian macrophages. Duplicate WT Listeria monocytogenes (strains 10403S and LO28) were used to infect mouse bone marrow-derived macrophages (BMMs). Bacterial RNA was harvested at 4 hours post-infection.

2011-12-02 | E-GEOD-34083 | biostudies-arrayexpress

Transcriptome analysis in macrophages isolated from wild-type, Stat1Y701F or Stat1-/- mice infected with Listeria monocytogenes for 6, 12, or 24 hours

Project description:We infected the bone marrow-derived macrophages (BMDM) isolated from WT, Stat1Y701F or Stat1-/- mice were infected with Listeria monocytogenes for 6, 12 or 24h, or left untreated in order to find out how the transcriptome of these genotypes differs during infection.

2016-01-26 | E-MTAB-3598 | biostudies-arrayexpress

Time-course of bone marrow macrophages infected with Listeria monocytogenes in the presence or absence of IFNgamma

Project description:Bone marrow derived macrophages from C57BL/6 or C57BL/6-Sst1S strains of mice were pretreated ± 100U/ml interferon gamma then infected for 0, 1, 2, 4, or 6h with Listeria monocytogenes. C57BL/6-Sst1S mice carry the Sst1 chromosomal locus of C3H mice. The Sst1 locus controls susceptibility to intracellular pathogens - these mice are therefore more susceptible than wild type B6.

2017-06-30 | E-MTAB-5784 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow derived macrophages

Project description:Macrophages phagocytose bacteria. Certain pathogenic bacteria access and replicate within the cytosol of infected macrophages and induce changes in macrophage gene expression by triggering of innate immune receptors and/or the effects of bacterial virulence factors. We used microarray analysis to identify changes in macrophage gene expression following infection with Listeria monocytogenes. Experiment Overall Design: Macrophages were cultured from bone marrow of female C57BL/6 mice using 10% L-cell conditioned media and mock infected (3 chips) or infected with log phase L. monocytogenes (2 chips). Samples were harvested for RNA isolation at 10 h after infection. Experiment Overall Design: Supplementary file below reports Genesifter-processed data: mean ("P" only) signal intensities and SEM for the MOCK and LM_INF groups.

2010-01-23 | E-GEOD-19374 | biostudies-arrayexpress

RNA-Seq profiling of ERCC1-XPF DNA repair defect (Er1F/-) versus wild type (Er1F/+) macrophages

Project description:DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) riggers Golgi dispersal, dilation of endoplasmic reticulum, autophagy and exosome biogenesis leading to the secretion of extracellular vesicles (EVs) in vivo and ex vivo.

2019-11-04 | E-MTAB-8439 | biostudies-arrayexpress

Misregulation of the broad-range phospholipase C activity increases the susceptibility of Listeria monocytogenes to intracellular killing by neutrophils

Project description:Listeria monocytogenes is a facultative intracellular bacterial pathogen that tightly regulates the activities of various virulence factors during infection. A mutant strain (the plcBM-NM-^Tpro mutant) that has lost the ability to control the activity of a phospholipase C (PC-PLC) is attenuated a hundred fold in mice. This attenuation is not due to a lack of bacterial fitness, but appears to result from a modified host response to infection. The transcriptomic pattern of immunerelated genes in infected macrophages indicated no differential response to wild-type L. monocytogenes vs the plcBM-NM-^Tpro mutant. Cultures of bone marrow derived macrophages from BALB/c were infected with either wild type or mutant L. monocytogens for 3, 6, or 9 hrs. The macrophages were then collected and RNA isolated for microarray analysis of gene expression.

2013-08-14 | E-GEOD-49820 | biostudies-arrayexpress

Transcriptome analysis in macrophages treated with type I interferon, heat-killed Listeria monocytogenes, or both.

Project description:To define the group of genes which is synergistically induced by cooperative activity of the type I interferon - activated Jak/STAT pathway and other pathways, we treated bone marrow-derived macrophages (BMDM) with heat-killed Listeria (hkL; non-STAT pathways activated), type I interferon alone (only STAT pathway activated), or both stimuli together.

2015-06-15 | E-MTAB-3015 | biostudies-arrayexpress

Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity

Project description:The transcription factor STAT1 is essential for interferon- (IFN) mediated protective immunity in humans and mice. Two splice isoforms of STAT1, STAT1M-NM-1 and STAT1M-NM-2, differ with regard to a C-terminal transactivation domain, which is absent in STAT1M-NM-2. Dimers of STAT1M-NM-2 are therefore considered transcriptionally inactive and potential competitive inhibitors of STAT1M-NM-1. Contrasting this view, generation and analysis of mice deficient for either STAT1M-NM-1 or STAT1M-NM-2 demonstrated transcriptional activity of the STAT1M-NM-2 isoform and its enhancement of innate immunity. Gene expression profiling in primary cells revealed overlapping, but also non-redundant and gene-specific activities of STAT1M-NM-1 and STAT1M-NM-2 in response to IFNM-NM-3. Consistently, both isoforms mediated protective, IFNM-NM-3-dependent immunity against the bacterium Listeria monocytogenes, although with remarkably different efficiency. In contrast, STAT1M-NM-1 and STAT1M-NM-2 were largely redundant for transcriptional responses to IFNM-NM-1/M-NM-2 and for IFNM-NM-1/M-NM-2-dependent antiviral activity. Collectively, our data shed new light on how STAT1 isoforms contribute to antimicrobial immunity. We treated macrophages of Stat1 delta alpha and Stat1 delta beta isoforms as well as Stat1 KO and Stat1 Wt mice with IFN gamma and Listeria to reveal differences in gene expression between isoforms and the two control genotypes.

2014-04-04 | E-GEOD-48970 | biostudies-arrayexpress

MiR expression profile in M1-polarized bone marrow derived macrophage cells compared with normal mouse aortic tissue.

Project description:The global change of the miR expression profile during atherosclerosis is due to the infiltration of different types of leukocytes into the arterail vessel wall in addition to disease-specific regulation in vascular cells. Monocyte-derived macrophage accumulation in the subintimal region is critical in the formation of atherosclerotic plaques. It is currently unknown which miRs are involved in the atherogenic macrophage response. The comparison of the miR expression profile in LPS/Interferon-gamma activated mouse macrophages with the miR expression in the normal aortic vessel wall was performed to detect macrophage-enriched miRs. This screening may help to identify macrophage-enriched miRs in atherosclerotic vessels that may play a role in the macrophage function during atherogenesis. Bone marrow cells were harvested from femura of 6-8 week old female C57BL/6 mice, re-suspended in DMEM-F12/10% FCS/10% L929-conditioned medium, and cultured for 7 days to differentiate into primary macrophages. F4/80 and CD11b expression was determined by flow cytometry to confirm the macrophage phenotype. Macrophages were stimulated with LPS (100ng/ml, 14 hours) and INF-g (10ng/ml, 6 hours) and the M1 polarization was verified by quantification of mannose receptor C type 1 (MRC1), arginase II (ArgII), inducible nitric oxide synthase (iNOS), and arginase I (ArgI) by qRT-PCR. Total RNA (M1-type macrophages and aorta tissue) was isolated using mirVana microRNA Isolation Kit.

2014-01-01 | E-GEOD-26556 | biostudies-arrayexpress

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