Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260167 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The mass spectrometry data describes the phosphorylation of a transcription factor known as interferon regulatory factor 9 (IRF9), under IFNbeta-induced or non-induced conditions. IRF9 is involved in the transcriptional regulation of hundreds of interferon-stimulated genes as part of the innate immune response.
2022-07-20 | MSV000089924 | MassIVE
Project description:Wang et al. identify MARK2 as a key regulator of innate antiviral immunity. The phosphorylation of GEF-H1 at Ser645 by MARK2 enhances TBK1 activation and induces IFN-β and interferon-stimulated genes. This establishes the MARK2–GEF-H1–TBK1 axis as a fundamental component of host antiviral defense.
2025-12-15 | PXD071998 |
Project description:Innate immune responses induce hundreds of interferon-stimulated genes (ISGs), many of which play an important role in antiviral immunity. Viperin, a member of the radical SAM superfamily of enzymes, is the product of one such ISG and it restricts the replication of a broad spectrum of DNA and RNA viruses. However, a general mechanism that explains all the roles proposed for viperin in the innate immune response remains to be defined. Here we report a previously unknown antiviral mechanism, in which viperin represses translation of viral RNA. We show that viperin interacts with the translation machinery and, primarily through its radical SAM enzymatic activity, inhibits global translation during the interferon response by activating the eIF2 pathway. In cell based-infection assays, viperin inhibits viral protein synthesis and viral replication of Zika virus and Kunjin virus. This study illustrates the importance of translational repression in the antiviral response and identifies viperin as a central translational regulator in innate immunity.
2022-05-22 | GSE142015 | GEO
Project description:The interferon response is a signaling pathway unique to vertebrates that links the innate and adaptive immune responses. Interferons signal through a cascade of factors including the JAK-STAT pathway to induce the transcription of hundreds of interferon stimulated genes (ISGs). Although the main interferon signal transduction pathways and ISGs have been elucidated, translational regulation of ISG transcripts has not been fully investigated. Prior work demonstrated that ribosomal protein RPL28 negatively regulates a subset of ISGs; however, we find that this effect may be due to a reduction in overall ribosome availability. Multi-omics analysis of RNA-seq and LC-MS/MS data reveal proteins that are translationally up-regulated in IFN-β-stimulated cells depleted of ribosome biogeneis factor BOP1, including an enrichment of ISGs. Analysis of codon usage demonstrates a significant reduction in codon optimality for proteins that are translationally up-regulated during BOP1 knockdown and IFN-β stimulation. Using reporter constructs, we demonstrate that codon non-optimal reporters are translated more that codon-optimized reporters in BOP1-depleted IFN-β cells. We propose that ribosome biogenesis regulates translational fine-tuning of integral protein production to ensure optimal interferon responses.
2026-04-30 | PXD060209 | Pride
Project description:Wild type HIV-1 can infect macrophages to establish productive infection without triggering innate immune receptors or type 1 interferon responses that would otherwise restrict virus propagation. We found that HIV-1 capsid mutants that disrupt capsid interactions with two host factors CPSF6 and cyclophillin A do not replicate in macrophages because they do trigger interferon responses. Genome-wide transcriptional profiling was used to compare the repertoire of interferon stimulated genes induced by these capsid mutants after 24Êh with stimulation of macrophages with interferon-beta or with the RNA analogue Poly IC.
2014-02-12 | E-MTAB-1437 | biostudies-arrayexpress
Project description:Amyloid beta (Aβ) plaque deposition in the central nervous system (CNS) is a hallmark of Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA), triggering an innate immune response. However, the role of the adaptive immune system is less clear. We investigated immune microenvironment dynamics in APP23 transgenic (APP23-tg) mice modelling CNS amyloid pathology, using single-cell transcriptomics. A significant increase in T-cell populations, particularly CD8+ T-cells, was observed in late stages, clustering around Aβ plaques, indicating a targeted response. A novel Aβ plaque-associated subset of CD8+ T-cells expressing interferon-stimulated genes (ISGs), was found to drive Type-I interferon responses. This subset also produced CXCL10, which mediated non-ISG T-cell trafficking via the CXCL10-CXCR3 axis. Importantly, we corroborated our observations by identifying similar Type-I interferon responses near plaques in human CNS amyloid pathology. These findings highlight a shift from microglia-driven to T-cell-mediated neuroinflammation as amyloid pathology progresses, with implications for time-resolved therapy development.
2026-01-01 | GSE280018 | GEO
Project description:The interferon Stimulated Gene-15 (ISG15) is a ubiquitin-like modifier induced by type I Interferon (IFN-I) and plays a crucial role in the innate immune response against viral infections. ISG15 is conjugated to target proteins by an enzymatic cascade through a process called ISGylation. While USP18 is a well-defined deISGylase counteracting ISG15 conjugation, ISG15 cross-reactive deubiquitylating enzymes (DUBs) have also been reported. Our study reports USP24 as a novel ISG15 cross-reactive DUB identified through activity-based protein profiling (ABPP). We demonstrated that recombinant USP24 processed pro-ISG15 and ISG15-linked synthetic substrates in vitro. Moreover, the depletion of USP24 significantly increased the accumulation of ISG15 conjugates upon IFN-β stimulation. An extensive proteomic analysis of the USP24-dependent ISGylome, integrating total proteome, GG-peptidome, and ISG15 interactome data, identified MOV10 as a specific target of USP24 for deISGylation. Further validation in cells revealed that ISGylated MOV10 enhances IFN-β production, whereas USP24 deISGylates MOV10 to negatively regulate the innate immune response. This study showcase USP24's novel roles in modulating ISGylation, IFN-I production, and innate immune responses with therapeutic implications in infectious diseases, cancer, autoimmunity, and neuroinflammation.
2026-05-13 | PXD055843 | Pride
Project description:Dendritic cells (DC) play a pivotal regulatory role in activation of the innate as well as the adaptive part of the immune system by responding to environmental microorganisms. We have previously shown that some lactobacilli strains induce a strong production of the pro-inflammatory and Th1 polarizing cytokine IL-12 in DC. Contrary, bifidobacteria do not induce IL-12, but are able to inhibit the IL-12 production induced by lactobacilli. In the present study, genome wide microarrays were used to investigate the maturation and gene expression pattern murine bone marrow derived DC stimulated with Lactobacillus acidophilus NCFM and Bifidobacterium bifidum Z9. L. acidophilus NCFM strongly induced expression of interferon (IFN)-β, multiple virus defence genes, and cytokine and chemokine genes related to both the adaptive and the innate immune response. Contrary, B. bifidum Z9 mostly up-regulated genes encoding cytokines and chemokines related to the innate immune response. Moreover, B. bifidum Z9 inhibited the expression of the genes initiating the adaptive immune response induced by L. acidophilus NCFM and had an additive effect on genes of the innate immune response and some Th2 skewing genes. The gene encoding Jun dimerization protein 2 (JDP2), a key regulator in cell signalling, was one of the few genes only induced by B. bifidum Z9. Blocking of the JNK1/2 pathway completely inhibited the gene expression of Ifn-β. We suggest that B. bifidum Z9 employs an active mechanism to inhibit induction of genes in DC triggering the adaptive immune system and that JPD2 is involved in the regulatory mechanism. In the experiment saline control, Lactobacillus acidophilus NCFM, Bifidobacterium bifidum Z9 or both bacteria were were added to murine dendritic cells and stimulated for 10 hours. Experiments were run in triplicates and analyzed in a Two-way ANOVA design.
2010-02-24 | E-GEOD-20302 | biostudies-arrayexpress
Project description:The study shows that RLRs drive distinct immune gene activation and polarization of the immune response. In our data, the RLR-dependent, WNV-induced immune response polarization overshadows the classical drivers of viral innate immune responses, interferon I (IFN) and IFN-stimulated genes, thus underscoring the importance of innate immune activation for channeling the adaptive immune system into specific effector pathways
2019-02-01 | GSE104817 | GEO
Project description:Dendritic cells (DC) play a pivotal regulatory role in activation of the innate as well as the adaptive part of the immune system by responding to environmental microorganisms. We have previously shown that some lactobacilli strains induce a strong production of the pro-inflammatory and Th1 polarizing cytokine IL-12 in DC. Contrary, bifidobacteria do not induce IL-12, but are able to inhibit the IL-12 production induced by lactobacilli. In the present study, genome wide microarrays were used to investigate the maturation and gene expression pattern murine bone marrow derived DC stimulated with Lactobacillus acidophilus NCFM and Bifidobacterium bifidum Z9. L. acidophilus NCFM strongly induced expression of interferon (IFN)-β, multiple virus defence genes, and cytokine and chemokine genes related to both the adaptive and the innate immune response. Contrary, B. bifidum Z9 mostly up-regulated genes encoding cytokines and chemokines related to the innate immune response. Moreover, B. bifidum Z9 inhibited the expression of the genes initiating the adaptive immune response induced by L. acidophilus NCFM and had an additive effect on genes of the innate immune response and some Th2 skewing genes. The gene encoding Jun dimerization protein 2 (JDP2), a key regulator in cell signalling, was one of the few genes only induced by B. bifidum Z9. Blocking of the JNK1/2 pathway completely inhibited the gene expression of Ifn-β. We suggest that B. bifidum Z9 employs an active mechanism to inhibit induction of genes in DC triggering the adaptive immune system and that JPD2 is involved in the regulatory mechanism.
2010-02-13 | GSE20302 | GEO