IRF1 and IFNγ regulated gene expression in A549 lung epithelial cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE181861 | GEO | 2022/02/02
REPOSITORIES: GEO
Similar Datasets
Project description:IRF1 and IFNγ regulated gene expression in A549 lung epithelial cells
| PRJNA753768 | ENA
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
Project description:Analysis of transcriptional profiling change comparing A549 cells expressing control empty vector and A549 cells expressing Aiolos. Results provide insight into molecular mechanisms underlying functional consequence of ectopic expression of Aiolos in solid cancer cells. Two-condition experiment, A549-empty vs. A549-Aiolos cells. Biological replicates: 3 control, 3 transfected, independently grown and harvested. One replicate per array.
2013-09-13 | E-GEOD-50812 | biostudies-arrayexpress
Project description:Aims and methods: To analyze how IFNγ induces coding and non-coding nascent transcriptional changes, SNU-seq is used to measure genome-wide changes in nascent transcription in untreated, 0.5hr, 2hr and 24hr IFNγ treated Hep3B cells. SNU-seq identifies the last transcribed nucleotide at near single-nucleotide resolution. 3'-end RNA-seq is used to examine RNA levels. ChIPmentation and ATAC-seq are used to assess the differential chromatin landscape upon IFNγ treatments, measuring H3K27ac, H3K4me3 and CTCF genome-wide changes as well as DNA accessibility in untreated, 0.5hr, 2hr and 24hr IFNγ treated Hep3B cells. Higher-order chromatin structure is investigated upon IFNγ treatments using Capture-C to measure promoter interactions of three gene promoters; IRF1, STAT1, and CD274. Results: 3'-end RNA-seq reveals IFNγ stimulated genes. SNU-seq identifies dynamic transcription at genes and non-coding intergenic regions and is used to demonstrate differential APA upon IFNγ treatments. By measuring transcription at nucleosome depleted regions, differential enhancer activity was demonstrated. IFNγ induces hundreds of methylation changes and thousands of acetylation changes over 24hrs. Unlike H3K4me3 which is deposited at late timepoints, H3K27ac is dynamically deposited. This acetylation is sometimes sustained throughout 24hrs but is often transiently deposited. CTCF shows very few binding changes throughout the timecourse. IFNγ induces significant changes in promoter:enhancer interactions at IRF1 and STAT1. The CD274 promoter loops to the nearest gene promoter; PLGRKT.
2021-10-12 | GSE172053 | GEO
Project description:This experiment was designed to identify IFNg-regulated, IRF1-dependent genes during infection with the intracellular pathogen Shigella flexneri. WT and Irf1-/- MEFs were stimulated for 18 hours with IFNg or left unstimulated; all of the cells were subsequently infected for 6 hours with S. flexneri prior to harvest of total RNA.
2011-09-01 | E-MTAB-713 | biostudies-arrayexpress
Project description:The cytokine IFNγ differentially impacts on tumors upon immune checkpoint blockade (ICB). Despite our understanding of downstream signaling events, less is known about 36 regulation of its receptor (IFNγ-R1). With an unbiased genome-wide CRISPR/Cas9 screen for critical regulators of IFNγ-R1 cell surface abundance, we identified STUB1 as an E3 ubiquitin ligase for IFNγ-R1 in complex with its signal-relaying kinase JAK1. STUB1 mediates ubiquitination-dependent proteasomal degradation of IFNγ-R1/JAK1 complex through IFNγ-R1K285 and JAK1K249. Conversely, STUB1 inactivation amplifies IFNγ signaling, sensitizing tumor cells to cytotoxic T cells in vitro. This was corroborated by an anticorrelation between STUB1 expression and IFNγ response in ICB-treated patients. Consistent with the context-dependent effects of IFNγ in vivo, anti-PD-1 response was increased in heterogenous tumors comprising both wildtype and STUB1-deficient cells but not full STUB1 knockout tumors. These results uncover STUB1 as a critical regulator of IFNγ-R1, and highlight the context-dependency of STUB1-regulated IFNγ signaling for ICB outcome.
2022-03-07 | PXD030580 | Pride
Project description:We performed chromatin immnoprecipitation followed by sequencing (ChIP-Seq) of IRF1 in different LC cell lines.
2023-03-16 | GSE186168 | GEO
Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we performed chromatin immunoprecipitation with Irf1-specific antibodies in NMuMG cells treated for 2 days with TGFbeta or left untreated (0d TGFbeta). Intersection with RNA-sequencing after downregulation of Irf1 with or without treatment with TGFbeta for two days revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
2022-03-18 | GSE141501 | GEO
Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we downregulated Irf1 by siRNA and analyzed differentially regulated genes and pathways upon EMT induction (2 days TGFbeta) or in the absence of EMT (0 day TGFbeta). Intersection with Irf1 ChIP-sequencing after 2 days of TGFbeta treatment or in untreated cells revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
2022-03-18 | GSE141500 | GEO
Project description:Macrophages are highly dynamic innate immune cells that adopt temporary phenotypes, known as polarization states, in response to changing environmental signals to combat microbial infection and contribute to the maintenance of tissue homeostasis. During the early stages of an infection, exposure to interferon-gamma (IFNγ) and microbial ligands induce M1 polarization, a heightened proinflammatory anti-microbial state, by regulating the expression of interferon stimulated genes (ISGs). While this response must be sufficiently vigorous to ensure the successful clearance of invading pathogens, it must also be spatially and temporally restricted to prevent uncontrolled inflammation that could result in tissue damage and disease. This is controlled by a variety of cell-extrinsic and -intrinsic mechanisms, including the expression of CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl-terminal domain 2 (CITED2), a transcriptional coregulator that limits IFNγ-stimulated proinflammatory gene expression by inhibiting STAT1- and IRF1-regulated ISGs. In this study, we show that CITED1, another member of the CITED family of proteins, is itself an ISG and is expressed in a STAT1-dependent manner, and that IFNγ stimulates the nuclear accumulation of fluorescently tagged CITED1 proteins. In contrast to CITED2, ectopic expression of CITED1 enhanced the expression of a subset of ISGs, including Ccl2, Ifit3b, Isg15, and Oas2. This effect was reversed in a Cited1 null cell line produced by CRISPR-based genomic editing. Collectively, these data show that CITED1 helps to maintain proinflammatory gene expression during periods of prolonged IFNγ exposure and suggests a distinct and antagonistic relationship between CITED proteins in the regulation of macrophage inflammatory function.
2023-01-01 | GSE217961 | GEO