Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Properties of STAT1 and IRF1 Enhancers and the Influence of SNPs

ABSTRACT: Properties of STAT1 and IRF1 Enhancers and the Influence of SNPs

PROVIDER: PRJNA369441 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Properties of STAT1 and IRF1 enhancers and the influence of SNPs.

Project description:BackgroundSTAT1 and IRF1 collaborate to induce interferon-γ (IFNγ) stimulated genes (ISGs), but the extent to which they act alone or together is unclear. The effect of single nucleotide polymorphisms (SNPs) on in vivo binding is also largely unknown.ResultsWe show that IRF1 binds at proximal or distant ISG sites twice as often as STAT1, increasing to sixfold at the MHC class I locus. STAT1 almost always bound with IRF1, while most IRF1 binding events were isolated. Dual binding sites at remote or proximal enhancers distinguished ISGs that were responsive to IFNγ versus cell-specific resistant ISGs, which showed fewer and mainly single binding events. Surprisingly, inducibility in one cell type predicted ISG-responsiveness in other cells. Several dbSNPs overlapped with STAT1 and IRF1 binding motifs, and we developed methodology to rapidly assess their effects. We show that in silico prediction of SNP effects accurately reflects altered binding both in vitro and in vivo.ConclusionsThese data reveal broad cooperation between STAT1 and IRF1, explain cell type specific differences in ISG-responsiveness, and identify genetic variants that may participate in the pathogenesis of immune disorders.

| S-EPMC5343312 | biostudies-literature

Properties of STAT1 and IRF1 Enhancers and the Influence of SNPs

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-01-31 | GSE94357 | GEO

Identifying interactors of IRF1 and STAT1 during type I and type II interferon treatment using proximity-dependent labeling

Project description:Identifying interactors of IRF1 and STAT1 in bone marrow-derived macrophages during type I and type II interferon treatment using the proximity-dependent labeling approach TurboID followed by Mass Spectrometry

2024-03-12 | PXD040337 | Pride

STAT1 and IRF1 enrichment in naive and primed HeLa cells upon IFNγ treatment

Project description:STAT1 and IRF1 transcription factor enrichment by CUT&RUN. HeLa cells were primed with IFNγ for 24 hours, followed with IFNγ washout. After 48h, naïve and primed cells were induced by IFNγ for 1h and 3h. Cells were harvested at indicated time points and processed for CUT&RUN

2023-05-06 | E-MTAB-12625 | biostudies-arrayexpress

Impact of IRF1 on transcriptome changes in Huh-7 human hepatoma cells and STAT1-deficient human fibroblasts

Project description:IRF1, and interferon-induced transcription factor, was found to have antiviral activity against a range of viruses when overexpressed. To determine which genes are associated with expression of IRF1, gene expression analysis was carried out in two different cell line expressing IRF1. The results show that more than 100 genes, many of which overlap with type I interferon-stimulated genes, are induced more than 3-fold by IRF1. A majority of the genes were induced in both cell types, while some genes were highly induced in a cell type-specific manner. To investigate the impact of IRF1 overexpression on the transriptome of two target cell lines, cells were transduced with a lentiviral vector expressing IRF1 or Firefly luciferase (Fluc) as a control. Total mRNA was harvested 48 h post-transduction and processed for Illumina BeadArray analysis. Skin fibroblast cell line described in Dupuis, S. et al., Impaired response to interferon-alpha/beta and lethal viral disease in human STAT1 deficiency. Nat Genet 33 (3), 388 (2003)

2011-04-01 | E-GEOD-26817 | biostudies-arrayexpress

16MB binding of H3ac, H4ac, STAT1, IRF1 antibodies in IFNg treated and untreated HeLa cells using nimblegen array

Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 16MB gene locus(HG17) Keywords: ChIP-chip three replicates for each marker at each state.

2009-01-14 | E-GEOD-11131 | biostudies-arrayexpress

16MB binding of STAT1 and IRF1 transcription factors in IFNg treated and untreated HeLa cells using NimbleGen array

Project description:Analysis of STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucleotide probes at 30bp intervals tiling over non-repetitive 16MB gene locus (HG17).

2017-12-22 | GSE94352 | GEO

16MB binding of H3ac, H4ac, STAT1, IRF1 antibodies in IFNg treated and untreated HeLa cells using nimblegen array

2009-01-15 | GSE11131 | GEO

CIITA locus binding of H3ac, H4ac, STAT1, IRF1 antibodies in IFNg treated and untreated HeLa cells using nimblegen array

2008-04-15 | GSE10206 | GEO

IRF1 cooperates with ISGF3 or GAF to form innate immune de novo enhancers

Project description:Macrophages exposed to immune stimuli reprogram their epigenomes to alter their subsequent functions. Endotoxin exposure causes widespread nucleosome remodeling and formation of thousands of de novo enhancers. However, it remains unclear how signal-dependent transcription factors collaborate to remodel the epigenome. Here, we dissected the regulatory logic by which the network of interferon regulatory factors (IRFs) catalyzes the opening of chromatin and the formation of de novo enhancers. We found that endotoxin-activated IRF3 is directly responsible for the induction of few de novo enhancers but is broadly required indirectly through activation of type I interferon-induced ISGF3. However, ISGF3 has limited capacity to initiate enhancer formation by itself – it must cooperate with IRF1, particularly at locations where the chromatin is less accessible. At these locations, IRF1 is required for the initial opening of chromatin, with ISGF3 extending accessibility and promoting the deposition of H3K4me1, marking poised enhancers. Because IRF1 expression must be induced by NFκB, IRF-regulated enhancers require that both branches of the innate immune signaling network, IRF3 and NFκB, are activated. However, type II interferon, typically produced by T-cells, may also induce IRF1 via the STAT1 homodimer GAF. We show that in this context, IRF1 is also responsible for opening inaccessible chromatin sites that can then be exploited by GAF to form de novo enhancers. Our results reveal how combinatorial logic gates of IRF1-ISGF3 or IRF1-GAF restrict immune epigenomic memory formation to macrophages exposed to pathogen or IFNγ-secreting T cells, but not bystander macrophages exposed only to transient type I interferon.

2025-03-17 | GSE270507 | 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