Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenomic landscapes of human inflammation associated macrophages

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Joachim Schultze

PROVIDER: E-GEOD-66595 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The transcriptional regulator network of human inflammatory macrophages is defined by open chromatin.

Schmidt Susanne V SV Krebs Wolfgang W Ulas Thomas T Xue Jia J Baßler Kevin K Günther Patrick P Hardt Anna-Lena AL Schultze Hartmut H Sander Jil J Klee Kathrin K Theis Heidi H Kraut Michael M Beyer Marc M Schultze Joachim L JL

Cell research 20160105 2

Differentiation of inflammatory macrophages from monocytes is characterized by an orderly integration of epigenetic and transcriptional regulatory mechanisms guided by lineage-determining transcription factors such as PU.1. Further activation of macrophages leads to a stimulus- or microenvironment-specific signal integration with subsequent transcriptional control established by the action of tissue- or signal-associated transcription factors. Here, we assess four histone modifications during hu ...[more]

PMID: 26729620

Similar Datasets

Epigenomic landscapes of human inflammation associated macrophages [ChIP-seq]

Project description:We previously demonstrated by genomic and bioinformatical approaches that human macrophage (MÎ¦) activation is best described by a spectrum model (Xue et al, Immunity, 2014). MÎ¦ integrate exogenous input signals on transcriptional level in a unique fashion to generate specific functional programs, enabling the plasticity in disease-related pathophysiologies. Such versatile responsiveness requires fast changes of transcription mediated by transcriptional regulators (TRs) or epigenomic changes. To better understand the principles of this regulation during human MÎ¦ activation, we assessed histone modifications including H3K4me1, H3K4me3, H3K27me3, and H3K27Ac by ChIP-sequencing allowing us to characterize the functional state of promoters (active, poised, repressed) and enhancers (active, inactive, intermediate). Using transcriptome data from our MÎ¦ spectrum model, we generated a co-regulation network of all TRs. Next, we overlaid epigenomic information and transcriptional changes of major TRs over time onto the TR network. We observed that input signals like IFNÎ³ or TNFÎ± induce a specific network of TRs that are transcriptionally regulated themselves, the combination of regulated TRs changes over time with a boost of transcriptional regulation of dozens of TRs 4 to 12 hrs post input signal exposure, almost all TRs within the network show active promoters, even if the TR itself is not expressed, and similar results are obtained for enhancers with open or at least intermediated states. These findings strongly suggest that in MÎ¦, the TR-defined cellular â??switch panelâ?? is always accessible thereby allowing MÎ¦ to quickly respond to the diverse input signal repertoire from the environment. Epigenetic analysis of promoter and enhancer sites in primary human macrophage subtypes and correlation to RNA-seq expression data

2016-02-28 | E-GEOD-66594 | biostudies-arrayexpress

Epigenomic landscapes of human inflammation associated macrophages [RNA-seq]

Project description:We previously demonstrated by genomic and bioinformatical approaches that human macrophage (MÎ¦) activation is best described by a spectrum model (Xue et al, Immunity, 2014). MÎ¦ integrate exogenous input signals on transcriptional level in a unique fashion to generate specific functional programs, enabling the plasticity in disease-related pathophysiologies. Such versatile responsiveness requires fast changes of transcription mediated by transcriptional regulators (TRs) or epigenomic changes. To better understand the principles of this regulation during human MÎ¦ activation, we assessed histone modifications including H3K4me1, H3K4me3, H3K27me3, and H3K27Ac by ChIP-sequencing allowing us to characterize the functional state of promoters (active, poised, repressed) and enhancers (active, inactive, intermediate). Using transcriptome data from our MÎ¦ spectrum model, we generated a co-regulation network of all TRs. Next, we overlaid epigenomic information and transcriptional changes of major TRs over time onto the TR network. We observed that input signals like IFNÎ³ or TNFÎ± induce a specific network of TRs that are transcriptionally regulated themselves, the combination of regulated TRs changes over time with a boost of transcriptional regulation of dozens of TRs 4 to 12 hrs post input signal exposure, almost all TRs within the network show active promoters, even if the TR itself is not expressed, and similar results are obtained for enhancers with open or at least intermediated states. These findings strongly suggest that in MÎ¦, the TR-defined cellular âswitch panelâ is always accessible thereby allowing MÎ¦ to quickly respond to the diverse input signal repertoire from the environment. Epigenetic analysis of promoter and enhancer sites in primary human macrophage subtypes and correlation to RNA-seq expression data

2016-02-28 | E-GEOD-66593 | biostudies-arrayexpress

Discovery of Widespread Host Protein Interactions with the Pre-Replicated Genome of CHIKV using VIR-CLASP

Project description:The pioneer interactions between incoming viral RNA genomes and host proteins are crucial to infection and immune response. Until now, the ability to study these events was lacking. We developed VIR-CLASP (VIRal Cross-Linking And Solid-phase Purification) to characterize the earliest interactions between viral RNA and cellular proteins. We investigated the infection of human cells using Chikungunya virus (CHIKV) and Influenza A virus and identified hundreds of direct RNA-protein interactions. Here, we validate the biological impact of three protein classes that bind CHIKV RNA within minutes of infection. We find CHIKV RNA binds and hijacks the lipid-modifying enzyme FASN for pro-viral activity. We show that CHIKV genomes are N6-methyladenosine modified and that YTHDF1 binds and suppresses its replication. Finally, we find that the innate immune DNA sensor IFI16 associates with CHIKV RNA, reducing viral replication and maturation. Our findings have direct applicability to the investigation of potentially all RNA viruses.

2020-05-11 | PXD015863 | Pride

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [RNA-Seq]

Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. RNA-seq analysis of primary monocytes and macrophages from a QKI haploinsufficient patient and their (control) sibling.

2016-01-04 | E-GEOD-74978 | biostudies-arrayexpress

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-04 | E-GEOD-74979 | biostudies-arrayexpress

Transcription profiling of human cord blood derived CD34+ hematopoietic stem/progenitor cells to identifyTGF-beta1 target genes in human dendritic cells (DC).

Project description:CD34+ hematopoietic stem/progenitor cells were isolated from human cord blood and amplified in vitro for 10-14 days in serum-free medium with specific cytokines (Ju et al., Eur. J. Cell Biol. 82, 75-86, 2003; Hacker et al., Nat. Immunol. 4, 380-386, 2003). Cultured progenitor cells were induced to differentiate into DC in RPMI medium supplemented with 10% fetal calf serum, 2 mM L-glutamine, 0.1 microM Beta-mercaptoethanol, 100 U/ml penicillin and streptomycin (GIBCO-BRL) and 500 U/ml GM-CSF, 500 U/ml IL-4 for 6 days with or without 10 ng/ml TGF-beta1 as indicated (0.5x10E6 cells/ml). Every 2 days growth factors were added and cells were maintained at 0.5x10E6 cells/ml cell density. RNA was prepared and subjected to microarray analysis. Experiment Overall Design: Dendritic cells (DC) were treated for various periods of time (4, 16 and 36 hours) with TGF-beta1 (10 ng/ml) or left untreated. Experiment Overall Design: DC untreated Experiment Overall Design: DC + TGF-beta1 for 4 hours Experiment Overall Design: DC + TGF-beta1 for 16 hours Experiment Overall Design: DC + TGF-beta1 for 36 hours

2008-06-13 | E-GEOD-5151 | biostudies-arrayexpress

Identification and characterization of MCF01A circular RNAs [ChIP-seq]

Project description:Circular RNAs (circRNAs) are widespread circular forms of non-coding RNAs with largely unknown function. Because stimulation of mammary cells with the epidermal growth factor (EGF) leads to dynamic changes in the abundance of both coding and non-coding RNA molecules, and culminates in the acquisition of a robust migratory phenotype, this cellular model might disclose functions of circRNAs. Here we show that circRNAs of EGF-stimulated mammary cells are stably expressed, while mRNAs and micro-RNAs change within minutes. In general, the circRNAs we detected are relatively long-lived and weakly expressed. Interestingly, they are almost ubiquitously co-expressed with the corresponding linear transcripts, and the respective, shared promoter regions are more active compared to genes producing linear isoforms only. These findings imply that altered abundance of circRNAs, unlike changes in the levels of other RNAs, might not play critical roles in signaling cascades and downstream transcriptional networks that rapidly commit cells to specific outcomes. Histone 3 Lysine 27 Acetylation â 2 replicates

2015-12-17 | E-GEOD-71196 | biostudies-arrayexpress

Proteomic characterization of calcium macrophages

Project description:In this study, macrophages, which differentiated from monocytes due to exposure to calcium and no further growth factors, were characterized. For this purpose, their proteomic profile was compared to monocytes, M1 macrophages, M2 macrophages, DCs, and foam cells obtained from healthy donors or patients with rheumatoid arthritis (RA).

2022-02-17 | PXD026888 | Pride

Effects of high molecular weight phthalates on LPS-stimulated THP-1 macrophages - redoxome

Project description:In this study, the effects of three high molecular weight phthalates (DINP, DIDP, DPHP) and their metabolites (MHINP, MCINP, OHMPHP) were investigated in THP-1 macrophages. For this purpose, the redoxome, including overall as well as reversible cysteine oxidation, was evaluated.

2023-09-13 | PXD043139 | Pride

Effects of high molecular weight phthalates on LPS-stimulated THP-1 macrophages - proteome

2023-09-13 | PXD043025 | Pride