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Next Generation Sequencing Facilitates Quantitative Analysis of Genes expression profiles in ZNFX1 overexpression in Rig-I-/- cells with or without poly I:C stimulation

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Genes expression profiles in ZNFX1 overexpression in Rig-I-/- cells with or without poly I:C stimulation

PROVIDER: PRJNA549408 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9317860_1.fastq.gz	Fastqsanger.gz
	SRR9317860_2.fastq.gz	Fastqsanger.gz
	SRR9317857_1.fastq.gz	Fastqsanger.gz
	SRR9317857_2.fastq.gz	Fastqsanger.gz
	SRR9317858_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of Genes expression profiles in ZNFX1 overexpression in Rig-I-/- cells with or without poly I:C stimulation

Project description:Genes expression profiles in ZNFX1 overexpression in Rig-I-/- cells with or without poly I:C stimulation in A549 cells.

2019-08-30 | GSE132892 | GEO

Gene expression from splenic cells in response to VSV-M2 and ligands to RIG-I and MDA5

Project description:VSV-M2 is recognized by cytosolic RIG-I. Notably, 5'-triphosphate RNA molecules derived from either viral RNA or from the synthetically produced 3pRNA can also induce RIG-I activation. MDA5 stimulation is achieved using complexed poly(I:C), a synthetic analog of viral dsRNA. To test whether the RIG-I and MDA5 ligands 3pRNA and poly(I:C) can be used in their complexed structures to decipher RNA virus-induced sickness behavior in vivo, we first compared the tissue-specific signaling pathways after systemic challenge with VSV-M2 and the RIG-I and MDA5 ligands, respectively. A whole-genome expression analysis using splenic cells was carried out using an Affymetrix Mouse Gene 2.1 ST Array.

2016-04-20 | GSE74015 | GEO

Transcriptome-wide analyses of early immune responses in lumpfish leukocytes upon stimulation with poly(I:C)

Project description:Both bacterial and viral diseases are a major threat to farmed fish, as well as wild fish. As the antiviral immune mechanisms in lumpfish (Cyclopterus lumpus L.) are poorly understood, lumpfish leukocytes were stimulated with poly(I:C), a synthetic analog of virus dsRNA, and RNA sequencing was performed. Immune genes were identified, and transcriptome-wide analyses of early immune responses in lumpfish leukocytes showed that 310 and 1872 transcripts were significantly differentially expressed 6 and 24 hours post exposure (hpe) to poly(I:C), respectively. The most enriched GO terms when time had been accounted for, were immune system processes (GO:0002376) and immune response (GO:0006955). Analysis of differentially expressed genes (DEGs) showed that among the most highly upregulated genes were TLRs and genes belonging to the RIG-I signaling pathway, including LGP2, MDA5, TRIM25, STING, as well as IRF3, IL-8 and TNFα. RIG-I was not identified, but in silico analyses showed that genes encoding proteins involved in pathogen recognition, cell signaling, and cytokines of the TLR and RIG-I signaling pathway are mostly conserved in lumpfish when compared to mammals and other teleost species. Our analyses unravel the innate immune pathways playing a major role in antiviral defence in lumpfish. The information gathered can be used to compare research findings and lay the groundwork for future functional analyses of immune and pathogenicity mechanisms. Such knowledge is also necessary for the development of immunoprophylactic measures for lumpfish, which is extensively cultivated for use as cleaner fish in the aquaculture for removal of sea lice from Atlantic salmon (Salmo salar).

2023-06-01 | E-MTAB-12884 | biostudies-arrayexpress

Gene expression profile analysis of WT and LGP2-/- bone-marrow derived dendritic cells treated with a RIG-I agonist

Project description:We performed RNAseq analysis on WT and LGP2-/- BM-DCs treated with a RIG-I agonist (HCV Poly-U/C RNA) to understand how LGP2 impacts global transcriptional changes following activation of the RIG-I pathway. Analysis of the transcriptional profiles revealed that LGP2 functions as a negative regulator of RIG-I signaling as early as 1 hours post-RIG-I agonist treatment. This finding led us to study how LGP2 negatively influences RIG-I activation through post-translational modification.

2019-06-14 | GSE132696 | GEO

Gene expression changes upon activation of RIG-I by a minimal potent RIG-I ligand

Project description:We have developed highly potent synthetic activators of the vertebrate immune system that specifically target the RIG-I receptor. When introduced into mice, a family of short, triphosphorylated Stem Loop RNAs (SLRs) induces a potent interferon response and the activation of specific genes essential for antiviral defense. Using RNAseq, we provide the first in-vivo genome-wide view of the expression networks that are initiated upon RIG-I activation. We observe that SLRs specifically induce type I interferons, subsets of interferon-stimulated genes (ISGs), and cellular remodeling factors. By contrast, poly(I:C), which binds and activates multiple RNA sensors, induces type III interferons and several unique ISGs. The short length (10-14 base pairs) and robust function of SLRs in mice demonstrate that RIG-I forms active signaling complexes without oligomerizing on RNA. These findings demonstrate that SLRs are potent therapeutic and investigative tools for targeted modulation of the innate immune system.

2018-02-03 | GSE106229 | GEO

Differential RNASeq of human nasal epithelial cells stimulated with RIG-I ligand SLR14

Project description:The purpose of this study was to assess transcriptome changes in primary human airway epithelial cells following stimulation with RIG-I ligand.

2018-01-02 | GSE107898 | GEO

Differential RNASeq of human bronchial epithelial cells stimulated with RIG-I ligand SLR14

Project description:The purpose of this study was to assess transcriptome changes in primary human airway epithelial cells following stimulation with RIG-I ligand.

2018-08-17 | GSE107897 | GEO

The RNA Helicase DHX16 Provides Specific Viral RNA for RIG-I to Trigger Innate Antiviral Immunity

Project description:Type-I interferon (IFN-I) is essential to establish antiviral innate immunity. Unanchored (or free) polyubiquitin (poly-Ub) has been shown to regulate IFN-I responses, however few unanchored poly-Ub interactors are known. To identify factors regulated by unanchored poly-Ub in a physiological setting, we developed an approach to isolate unanchored poly-Ub from lung tissue and identified the DEAH-box RNA helicase DHX16 as a factor that enhances IFN-I production. Silencing of DHX16 in cells and in vivo diminished IFN-I responses against influenza virus. DHX16-dependent IFN-I production requires RIG-I and unanchored K48-poly-Ub synthesized by the E3 Ub ligase TRIM6. DHX16 recognizes a signal in influenza segments that undergo splicing and requires its intact RNA helicase motif for direct, high-affinity interactions with specific viral RNAs. Our study establishes DHX16 as a potentiator of RIG-I-mediated IFN-I production and recognizes a mechanism for activation of antiviral immunity requiring unanchored poly-Ub and the viral RNA recognition activity of DHX16

2022-03-08 | GSE168255 | GEO

KAP1-mediated epigenetic suppression in anti-RNA viral responses by direct targeting RIG-I and MDA5

Project description:Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), including RIG-I (encoded by Ddx58) and MDA5 (melanoma-differentiation-associated gene 5, encoded by Ifih1), are crucial for initiating antiviral responses. Endogenous retroviral elements (ERVs) are transposable elements derived from exogenous retrovirus that integrated into the genome. KRAB-associated protein 1 (KAP1) is a master epigenetic suppressor of ERVs, and thereby protects cells from detrimental genome instability. Increased ERV transcripts are sensed by RLRs and trigger innate immune signaling. However, whether KAP1 could directly control RLRs activity remain unclear. Here we show that KAP1 attenuates RNA viral infection induced type I IFNs and facilitates viral replication by inhibiting RIG-I/MDA5 expression in primary peritoneal macrophages of C57BL/6J mice. Kap1 deficiency increased IFN-β expression and inhibited VSV replication in C57BL/6J mice in vivo. Mechanistically, KAP1 binds to the promoter regions of Ddx58 and Ifih1, and promotes the establishment of repressive histone marks in primary peritoneal macrophages of C57BL/6J mice. Concordantly, KAP1 suppresses the expression of RIG-I and MDA5 at transcriptional level in primary peritoneal macrophages of C57BL/6J mice. Our results establish that KAP1 epigenetically suppresses host antiviral responses by direct targeting RIG-1 and MDA5, and thus facilitates the immune escape of RNA viruses.

2021-07-28 | GSE178443 | GEO

Proximity labeling proteins differences between TRIM25 and G3BP1 interactions or not, and Proximity labeling proteins differences between G3BP1 and TRIM25 in the presence or absence of poly(I:C) stimulation

Project description:This project investigates G3BP1 proximity proteins by constructing a G3BP1-BirA* fusion protein using G3BP1 as a decoy protein and BirA* as a biotin ligase. The changes in G3BP1 proximity proteins were studied in the presence or absence of poly(I:C) stimulation conditions, using poly(I:C) stimulation as a variable. This project investigated the TRIM25 proximity protein by constructing a TRIM25-BirA* fusion protein with TRIM25 as the decoy protein and BirA* as the biotin ligase. The changes of TRIM25 proximity proteins under the conditions of TRIM25 interacting with or without G3BP1 were studied by performing PTFG sequence deletion on TRIM25; the changes in TRIM25 proximity proteins were studied in the presence or absence of poly(I:C) stimulation conditions, using poly(I:C) stimulation as a variable.

2023-07-07 | PXD043603 |

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