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The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

ABSTRACT: The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

PROVIDER: PRJNA593669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10590626.fastq.gz	Fastqsanger.gz
	SRR10590627.fastq.gz	Fastqsanger.gz
	SRR10590628.fastq.gz	Fastqsanger.gz
	SRR10590629.fastq.gz	Fastqsanger.gz
	SRR10590630.fastq.gz	Fastqsanger.gz

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The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

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

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

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

The dual role of Irf1 in maintaining epithelial identity while enabling EMT

Project description:The dual role of Irf1 in maintaining epithelial identity while enabling EMT

| PRJNA593667 | ENA

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

Project description:The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

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The dual role of Irf1 in maintaining epithelial identity while enabling EMT

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

2022-03-19 | GSE141502 | GEO

Foxf2 plays a dual role during TGFb-induced EMT by promoting apoptosis yet enabling cell junction dissolution and migration.

Project description:We have identified the transcription factor forkhead box protein F2 (Foxf2) to be upregulated in its expression during the EMT process and studied its functional contribution to EMT by siRNA-mediated knockdown in NMuMG cells treated for 4 days with TGFbeta followed by mRNA-sequencing. Our analysis revealed a dual role of Foxf2 during TGFbeta-induced EMT in promoting apoptosis while inducing cell junction breakdown and migration.

2018-10-09 | GSE112796 | GEO

Foxf2 plays a dual role during TGFb-induced EMT by promoting apoptosis yet enabling cell junction dissolution and migration.

Project description:Foxf2 plays a dual role during TGFb-induced EMT by promoting apoptosis yet enabling cell junction dissolution and migration.

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Oncogenic Ras inhibits IRF1 to promote viral oncolysis

Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).

2014-11-13 | E-GEOD-49469 | biostudies-arrayexpress

IRF1 mass-spectrometry primary fibroblasts non-stimulated or stimulated with IFNg for 24h

Project description:Inborn errors of human IFN-γ immunity underlie mycobacterial diseases, whereas inborn errors of IFN-a/b immunity underlie viral diseases. Both types of IFNs induce the transcription factor IRF1. We describe two unrelated children with inherited complete IRF1 deficiency and early-onset, multiple, life-threatening diseases caused by weakly virulent mycobacteria. These children have no history of severe viral disease, despite exposure to many viruses, including SARS-CoV-2, which is life-threatening in individuals with impaired IFN-a/b immunity. The IRF1-dependent cellular responses to IFN-γ are, both quantitatively and qualitatively, much greater than those to IFN-a/b in vitro. Monocyte- and iPSC-derived macrophages from the two patients show no upregulation of at least 20% of the target genes normally induced by IFN-γ. By contrast, cell-intrinsic IFN-a/b immunity to diverse viruses, including SARS-CoV-2, is intact. Human IRF1 is, thus, largely redundant for antiviral IFN-a/b immunity. By contrast, human IRF1 is essential for IFN-γ immunity to mycobacteria in myeloid cells.

2023-01-19 | PXD037759 | Pride

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

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