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  1. 20141
    “…Our analysis identified CCL8, CXCL10, CXCL11, MxA, OAS2, and OAS1 as top contributing genes, all of which are stimulated by type I interferon. …”
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  2. 20142
    “…Then, IFIT1, RSAD2, IFIT3, USP18, ISG15, OASL, MX1, OAS2, OAS3, and IFI44 were considered to be hub ISGs in SLE by “MCODE” and “Cytohubba” plugins of Cytoscape, Moreover, the results of expression correlation suggested that 3 lncRNAs (NRIR, FAM225A, and LY6E-DT) were closely related to the IFN pathway. …”
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  3. 20143
  4. 20144
    “…RS model containing three prognostically significant M1 macrophage-associated genes (FBXO6, OAS1, and TMEM229B) was formed by multiple Cox analysis, and a polygenic risk model and a comprehensive prognostic line plot was developed. …”
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  5. 20145
    “…Six SNPs in NLRP3, TNF, OAS1, IL12B, and CTLA4 were associated with high responders with serum antibody titer > 4000 BAU/ml as boosting effect at 3 weeks after the second vaccination. …”
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  6. 20146
    “…Polymorphisms in the following candidate genes IL28B, IL6, IL10, TNFα, IFNγ, CCL5, MxA, OAS1, SOCS3, CTLA4 and ITPA were assessed. Genotyping was carried out using Sequenom iPLEX-Gold, a single-base extension polymerase chain reaction. …”
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  7. 20147
    “…BACKGROUND: Escherichia coli has two L-cysteine biosynthetic pathways; one is synthesized from O-acetyl L-serine (OAS) and sulfate by L-cysteine synthase (CysK), and another is produced via S-sulfocysteine (SSC) from OAS and thiosulfate by SSC synthase (CysM). …”
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  8. 20148
  9. 20149
    “…In 1 Mb windows surrounding the six significant QTL, we found 149 genes from which OAS2, STC2, SHOX, XKR4, and SGMS1 were the closest to the most significant QTL on BTA17, BTA20, BTA1, BTA14, and BTA26, respectively. …”
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  10. 20150
    “…For studying the relative expression of immuno-stimulatory genes (IFN-α, IFN-β, IFN-γ, IL-1β, iNOS and OAS) in CAM, TLR ligands were administered through intra-allantoicroute and CAM were collected at 4, 8 and 16 h post treatment. …”
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  11. 20151
    “…RESULTS: From the deQTL meta-analysis of the two ancestral populations, we identified significant cis-deQTLs for 15 genes (TBC1D4, MDGA1, CHI3L2, OAS1, GATM, ASNSD1, GLUL, TDRD12, PPIP5K2, OAS3, SERPINB1, ANKDD1A, DTD1, CYFIP2, and GSDME), eight of which were significant in at least one of the ancestry subsets alone. …”
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  12. 20152
  13. 20153
    “…These results further verified that peripheral blood mRNA expression levels of OAS1, IFIT1 and IFIT3 were significantly higher in PTB patients than HCs (all P < 0.01). …”
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  14. 20154
    “…VP3, the viral capping enzyme, utilizes a 2H-phosphodiesterase domain to prevent activation of the cellular oligoadenylate synthase (OAS)/RNase L pathway. Computational, molecular, and biochemical studies have provided key insights into the structural and mechanistic basis of innate immune antagonism by NSP1 and VP3 of group A rotaviruses (RVA). …”
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  15. 20155
    “…Overexpression of TRIM4 increased the mRNA levels of interferon (IFN)-alpha, IFN-beta, RIG-I, MAVS, IRF3, IRF7, OAS1, IFIT3, and CCL5, TRIM4 up-regulated the activities of IFN-beta, NF-κB, and ISRE reporter. …”
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  16. 20156
    “…The experiment was carried out over 28 days with replicates that were sacrificed on Days 0, 0.5, 3, 7, 14, 21 and 28. For the OAS and OASD treatments, abiotic weathering (i.e., evaporation) dominated the weathering process. …”
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  17. 20157
    “…The external datasets validated the upregulation of four interferon-related genes (OAS1, IFITM3, GBP1, and GBP2) in JAK2V617F (+) myelofibrosis. …”
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  18. 20158
    “…Specifically, levels of cytokine IL-21, cell surface receptor CD44, and intracellular molecules PP2A and OAS2 increased following Syk overexpression in normal T cells and decreased after Syk silencing in SLE T cells. …”
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  19. 20159
    “…EPSTI1 can activate PKR promoter and induce several PKR-dependent genes, including IFN-β, IFIT1, OAS1, and RNase L, which is responsible for EPSTI1-mediated antiviral activity.…”
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  20. 20160
    “…Mechanistically, DNA transfection activates the cGAS-STING pathway and induces the expression of the OAS family proteins, leading to the activation of RNaseL and degradation of mRNA derived from transgenes. …”
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