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

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

PROVIDER: PRJNA418284 | ENA |

REPOSITORIES: ENA

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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.

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

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

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A minimal RNA ligand for potent RIG-I activation in living mice.

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 RNA sequencing, 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, polyinosinic:polycytidylic acid [poly(I:C)], which binds and activates multiple RNA sensors, induces type III interferons and several unique ISGs. The short length (10 to 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.

| S-EPMC5821489 | biostudies-literature

RNA-seq comparison of gene induction in RIG-I stimulated old and young human monocytes

Project description:Goal: The goal of this study was to compare gene induction in old and young human monocytes upon stimulation of these cells with a RIG-I specific ligand, based on previously published results which indicated impaired interferon responses in monocytes from older individuals upon influenza virus infeciton.

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

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

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

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Nociceptin/orphanin FQ opioid receptor selective ligand MCOPPB as a potent senolytic drug

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Identification of avian RIG-I responsive genes during influenza infection

Project description:Transcriptional profiling of chicken embryonic fibroblasts (DF-1 cells) comparing the effects of chicken cells transfected with duck RIG-I compared to empty-vector transfected cells following with low or highly pathogenic avian influenza. Goal was to determine the effects of duck RIG-I on influenza-induced immune gene expression. Two-condition experiment. Biological replicates for low pathogenic avian influenza infection: 3 empty-vector transfected replicates, 3 RIG-I transfected replicates. Biological replicates for highly pathogenic influenza infection: 2 empty-vector transfected replicates, 2 RIG-I transfected replicates.

2012-12-12 | E-GEOD-29596 | biostudies-arrayexpress

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