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MRNAseq profiling of interferon-a stimulated WT and ISG15 KO- Human-iPSC derived macrophages

ABSTRACT: mRNAseq profiling of interferon-a stimulated WT and ISG15 KO- Human-iPSC derived macrophages

PROVIDER: PRJNA714055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13952747_1.fastq.gz	Fastqsanger.gz
	SRR13952747_2.fastq.gz	Fastqsanger.gz
	SRR13952748_1.fastq.gz	Fastqsanger.gz
	SRR13952748_2.fastq.gz	Fastqsanger.gz
	SRR13952749_1.fastq.gz	Fastqsanger.gz

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mRNAseq profiling of interferon-a stimulated WT and ISG15 KO- Human-iPSC derived macrophages

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10x single-cell RNAseq profiling of hiPSC derived WT and ISG15 KO macrophages stimulated with interferon-a and treated with itaconic acid, 4-octyl itaconate and ruxolitinib

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Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived brain microvascular endotheial cells to identify alterations in gene expression. Methods: RNA were isolated from HD and control iPSC-derived brain microvascular endothelial cells. mRNAseq using Illumina TruSeq mRNA PolyA+ v2 lib prep and HiSeq 2500. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis. Results: mRNAseq and statistical analysis revealed differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells. Conclusions: Our study shows differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells, and reveals gene networks that are relevant to the mechanism of HD pathogenesis.

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Project description:We assessed how lack of ISG15 influences the levels of transcripts after IFNa stimulation. Expression data from ISG15 deficient patients (P1, P2, P3) and control (C1, C6, C16) hTert fibroblasts

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Expression data from WT and ISG15 KO HaCaT cells stimulated with interferon-a and treated with combination treatment of Ruxolitinib, TGFb and Doxycycline

Project description:Analysis of gene expression in WT and ISG15 KO HaCaT cells, stimulated with IFNa and treated with ruxolitinib (RUX), transforming growth factor beta (TGFb) and doxycycline (DOXY) to investigate the effects of treatments on transcriptional response in the cells.

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Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

Project description:DNA replication and repair defects or genotoxic treatments trigger interferon (IFN)-mediated inflammatory responses. However, whether and how IFN signaling in turn impacts the DNA replication process has remained elusive. Here we show that basal levels of the IFN-stimulated gene 15, ISG15, and its conjugation (ISGylation) are essential to protect nascent DNA from degradation. Moreover, IFN treatment restores replication fork stability in BRCA1/2-deficient cells, which strictly depends on topoisomerase-1, and rescues lethality of BRCA2-deficient mouse embryonic stem cells. Although IFN activates hundreds of genes, these effects are specifically mediated by ISG15 and ISGylation, as their inactivation suppresses the impact of IFN on DNA replication. ISG15 depletion significantly reduces cell proliferation rates in human BRCA1-mutated triple-negative, whereas its upregulation results in increased resistance to the chemotherapeutic drug cisplatin in mouse BRCA2-deficient breast cancer cells, respectively. Accordingly, cells carrying BRCA1/2 defects consistently show increased ISG15 levels, which we propose as a novel, in-built mechanism of drug resistance linked to BRCAness.

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Project description:ISG15 is primarily documented as an interferon-stimulated, ubiquitin-like protein (ubl), which has anti-viral activity. Although ISG15 was the founding member of the ubl protein family, very little is known about its function. We have found that ISG15 expression in non-phagocytic cells is dramatically induced upon Listeria infection and that surprisingly this induction can be Type I Interferon independent. Listeria-mediated ISG15 induction depends on the cytosolic surveillance pathway, which senses bacterial DNA and signals through STING, TBK1, IRF3 and IRF7. Most importantly, we observed that ISG15 expression restricts Listeria infection both in vitro and in vivo. We then made use of Stable Isotope Labeling in tissue culture (SILAC) to identify the ISGylated proteins that could be responsible for the ISG15-mediated protective effect. Our SILAC analysis revealed that overexpression of ISG15 leads to a striking ISGylation of integral membrane proteins of the endoplasmic reticulum and Golgi apparatus, which correlates with increased canonical secretion of cytokines. Taken together, our data reveal a previously uncharacterized signaling pathway that restricts Listeria infection and acts via ISGylation, reinforcing the view that ISG15 is a key component of the innate immune arsenal of the mammalian host.

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ISG15 counteracts Listeria monocytogenes infection

2015-07-24 | PXD001805 | Pride