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ILF3 contributes to the establishment of the antiviral type I interferon program

ABSTRACT: ILF3 contributes to the establishment of the antiviral type I interferon program

PROVIDER: PRJNA540790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9000470_1.fastq.gz	Fastqsanger.gz
	SRR9000470_2.fastq.gz	Fastqsanger.gz
	SRR9000471_1.fastq.gz	Fastqsanger.gz
	SRR9000471_2.fastq.gz	Fastqsanger.gz
	SRR9000472_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ILF3 contributes to the establishment of the antiviral type I interferon program.

Project description:Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1, and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised.

| S-EPMC7145544 | biostudies-literature

ILF3 contributes to the establishment of the antiviral type I interferon program

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

2019-10-25 | GSE130618 | GEO

Effect of ILF3 on translation during homeostasis and the antiviral response

2019-10-25 | GSE130742 | GEO

Effect of ILF3 depletion in HeLa cells on RNA steady state levels

2019-10-25 | GSE130595 | GEO

Effect of ILF3 on translation during homeostasis and the antiviral response

Project description:Effect of ILF3 on translation during homeostasis and the antiviral response

| PRJNA541267 | ENA

RIP-seq using ILF3 antibodies to reveal RNAs that binds to ILF3 protein

Project description:RNA pulldown assay showed that lncRNA UBE2CP3 could bind to ILF3 protein. In order to further verify the interaction between ILF3 and UBE2CP3, RNA Immunoprecipitation (RIP) assay was performed to identify the RNAs that binds to ILF3 protein. RIP-seq data verifies the interaction between ILF3 and UBE2CP3. Interestingly, UBE2CP3 could also binds to 3'UTR of IGFBP7 mRNA. Mechanismly, lncRNA UBE2CP3 and 3' UTR of IGFBP7 could forms an double-stranded RNA. Then, the RNA duplex could interact with the Double-Stranded RNA-Binding Protein ILF3.

2021-05-03 | GSE163815 | GEO

Genome-wide binding sites of NF90/ILF3 in K562 erythroleukemia cells

Project description:We used ChIP-seq to characterize the genome-wide binding sites of NF90/ILF3 in K562 erythroleukemia cells.

2018-03-01 | E-MTAB-6042 | biostudies-arrayexpress

Knockdown of ILF2/ILF3 (NF45/NF90) in the gastric cancer cell line SGC7901

Project description:Our data showed that lncRNA ELF3-AS1 could bind on the exon1 of ELF3-201 to form a double-stranded RNA molecule. This double-stranded RNA could interact with ILF2/ILF3 complex. To explore the biofunction of the interaction between ELF3-AS1 and ILF2/ILF3 complex, loss-of-function studies regarding ILF2 and ILF3 were performed in SGC7901 cell line. RNA sequencing studies showed that knockdown of ILF3 significantly decreased ELF3-AS1, while knockdown of ILF2 significantly increased ELF3-AS1 and NF90 expression. Our data revealed that ILF2/ILF3 complex interacted with ELF3-AS1/ELF3 double-stranded RNA and regulated their transcripts stability.

2021-10-01 | GSE161544 | GEO

Viral Mimicry by Endogenous Y-RNAs Contributes to Antiviral Immunity

Project description:Viral Mimicry by Endogenous Y-RNAs Contributes to Antiviral Immunity

| PRJNA556649 | ENA

Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma

Project description:Acquired resistance represents a critical clinical challenge to molecular targeted therapies such as tyrosine kinase inhibitors (TKIs) treatment in hepatocellular carcinoma (HCC). Therefore, it is urgent to explore new mechanisms and therapeutics that can overcome or delay resistance. Here, we identified a U.S. Food and Drug Administration (FDA)-approved pleuromutilin antibiotic that overcomes sorafenib resistance in HCC cell lines, cell line-derived xenograft (CDX) and hydrodynamic injection mouse models. We demonstrated that lefamulin targets and binds Interleukin Enhancer-binding Factor 3 (ILF3) to inhibit sorafenib-induced mitochondrial ribosomal protein L12 (MRPL12) upregulation. Mechanistically, lefamulin directly binds to Ala-99 of ILF3 and interferes with acetyltransferase general control non-depressible 5 (GCN5) and CREB binding protein (CBP) mediated acetylation of Lys-100, which disrupting the ILF3-mediated transcription of MRPL12 and subsequent mitochondrial biogenesis. Clinical data further confirmed that high ILF3 or MRPL12 expression was associated with poor survival and targeted therapy efficacy in HCC. Conclusively, our findings suggest that ILF3 is a potential therapeutic target for overcoming resistance to TKIs, and lefamulin may be a novel combination therapy strategy for HCC treatment with sorafenib and regorafenib.

2024-01-17 | GSE252988 | GEO

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