Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [ChIP-seq]

ABSTRACT: Massive reprogramming of the host alveolar macrophage transcriptome occurs during the initial stages of tuberculosis. In bovine tuberculosis, Mcobacterium bovis can persist and replicate within alveolar macrophages through varied mechanisms to subvert or exploit host immune responses ( REF). To determine how these transcriptional changes are regulated we performed ChIPseq analysis of H3K4 and H3K27 methylation, established histone tail markers associated with permissive and repressive chromatin states, respectively. These analyses were carried out in parallel with RNA polymerase II ChIPseq, RNAseq and small non-coding RNAseq. This meta data file refers to the ChIP-seq datasets.

ORGANISM(S): Bos taurus

PROVIDER: GSE116731 | GEO | 2019/07/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [miRNA-seq]

Project description:Massive reprogramming of the host alveolar macrophage transcriptome occurs during the initial stages of tuberculosis. In bovine tuberculosis, Mcobacterium bovis can persist and replicate within alveolar macrophages through varied mechanisms to subvert or exploit host immune responses ( REF). To determine how these transcriptional changes are regulated we performed ChIPseq analysis of H3K4 and H3K27 methylation, established histone tail markers associated with permissive and repressive chromatin states, respectively. These analyses were carried out in parallel with RNA polymerase II ChIPseq, RNAseq and small non-coding RNAseq. This meta data file refers to the miRNA-seq datasets.

2019-07-05 | GSE116733 | GEO

Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [RNA-seq]

2019-07-05 | GSE116732 | GEO

Secretome Analysis of Mycobacterial-infected Bovine Macrophages

Project description:Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis, a chronic granulomatous disease. Mtb is mostly restricted to humans and seldom causes disease in animals. M. bovis (Mbv) on the other hand causes tuberculosis in cows (bovine tuberculosis) and several wild animals. Each of these pathogens therefore has unique host adaptations and the host- and pathogen-specific factors driving this differential tropism still remain largely unknown. Here we profiled the secretomes of Mtb- and Mbv-infected bovine macrophages to characterise host-specific responses to each pathogen.

2021-03-11 | PXD017949 | Pride

Genomic mapping of cAMP receptor protein binding in relation to transcriptional start sites in Mycobacterium tuberculosis

Project description:In this study we have used ChIPseq analysis to perform comprehensive mapping of the binding profile of the cAMP receptor protein (CRPMt) of M. tuberculosis combined with RNAseq studies to further investigate the transcriptional response following crp gene deletion and under alternative growth conditions.

2014-06-24 | E-MTAB-2390 | biostudies-arrayexpress

Active Mycobacterium tuberculosis regulatory networks from alveolar macrophages of in vivo mouse infection uncovered by Path-seq

Project description:Transcriptional profiling of Mycobacterium tuberculosis mRNA enriched from host-pathogen samples from in vivo alveolar macrophages (Mus musculus).

2019-03-04 | GSE116394 | GEO

Mycobacterial tuberculosis infection in hypoxia-inducible factor-1alpha deficient macrophages

Project description:We herein found the strong expression of hypoxia-inducible factor-1α (HIF-1α) in tuberculosis granulomas and more rapid death of HIF-1α-conditional knockout mice than wild-type mice after M. tuberculosis infection. These results prompted us to investigate the role of HIF-1α in host defenses against infection. Bone-marrow derived macrophages from Wild-type (WT) mice and HIF-1α-conditional knockout (HIF-1 CKO) mice were infected with M tuberculosis H37Rv (multiplicity of infection = 0.5) for 12 h, and extracellular bacilli were removed from the macrophage culture medium. Cells were cultured for 4 days in the presence of 500 U/ml IFN-γ. In microarray analysis using Gene Chip Mouse Gene 1.0 ST Array, the expression of 757 and 1190 genes was ≥1.3-fold stronger and ≥0.77-fold weaker, respectively, in HIF-1 CKO than in WT.

2018-09-30 | E-MTAB-7244 | biostudies-arrayexpress

Mycobacterial p(1)-type ATPases mediate resistance to zinc poisoning in human macrophages.

Project description:Mycobacterium tuberculosis thrives within macrophages by residing in phagosomes and preventing them from maturing and fusing with lysosomes. A parallel transcriptional survey of intracellular mycobacteria and their host macrophages revealed signatures of heavy metal poisoning. In particular, mycobacterial genes encoding heavy metal efflux P-type ATPases CtpC, CtpG, and CtpV, and host cell metallothioneins and zinc exporter ZnT1, were induced during infection. Consistent with this pattern of gene modulation, we observed a burst of free zinc inside macrophages, and intraphagosomal zinc accumulation within a few hours postinfection. Zinc exposure led to rapid CtpC induction, and ctpC deficiency caused zinc retention within the mycobacterial cytoplasm, leading to impaired intracellular growth of the bacilli. Thus, the use of P(1)-type ATPases represents a M. tuberculosis strategy to neutralize the toxic effects of zinc in macrophages. We propose that heavy metal toxicity and its counteraction might represent yet another chapter in the host-microbe arms race. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-122]

2012-01-27 | E-BUGS-122 | biostudies-arrayexpress

Elucidating the effects of the macrophage environment on the efficacy of anti-mycobacterial drugs

Project description:We examined the transcriptional responses of intracellular M. tuberculosis exposed to different front-line drugs during macrophage infection. Our data reveal that Mtb experiences amplification of multiple host-derived pressures following drug exposure. The stresses from the host environment have a dominant impact on Mtb gene expression to the extent that the transcriptional profiles cluster according to environment, ie. broth vs host cell, rather than drug.

2016-02-21 | GSE62942 | GEO

Multifaceted dysfunction of infant airway macrophages in response to Mycobacterium tuberculosis

Project description:Infants are vulnerable to disseminated forms of tuberculosis and suffer disproportionately high morbidity and mortality, but the reasons for this are unknown. We hypothesized that since alveolar macrophages (AMs) are critical in the uptake and containment of Mycobacterium tuberculosis (Mtb) in the lung, their function may be impaired in early life. We developed a method of obtaining AMs during rigid bronchoscopy of healthy infants with suspected airway abnormality. RNAseq analysis of Mtb-stimulated AMs from 4 infants and 4 adults was performed.

2020-03-12 | E-MTAB-7679 | biostudies-arrayexpress

ASPSCR1-TFE3 reprograms transcription by organizing enhancers around hexameric VCP [Cell_lines_ChIP, FUUR1, FUUR1_VCP]

Project description:ChIPseq experiments identify that ASPSCR1-TFE3 defines active enhancers across the genome and co-distributes with VCP/p97. RNAseq after knock-down of ASPSCR1-TFE3 or VCP, inhibition of VCP, or overexpression of each in alveolar soft part sarcoma cell lines demonstrates their co-dependence. HiChIP defines chromatin conformations that surround ASPSCR1-TFE3 targets and are lost on VCP knock-down.

2023-01-01 | GSE162482 | GEO

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