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gene exp mx1 hs00895598 m1  (Thermo Fisher)
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Thermo Fisher gene exp mx1 hs00895598 m1
Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , <t>Mx1</t> , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.
Gene Exp Mx1 Hs00895598 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gene exp mx1 hs00895608 m1  (Thermo Fisher)
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Thermo Fisher gene exp mx1 hs00895608 m1
Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , <t>Mx1</t> , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.
Gene Exp Mx1 Hs00895608 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gene exp mx1 mm00487796 m1  (Thermo Fisher)
99
Thermo Fisher gene exp mx1 mm00487796 m1
Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , <t>Mx1</t> , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.
Gene Exp Mx1 Mm00487796 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gene exp mx1 rh02842279 m1  (Thermo Fisher)
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Thermo Fisher gene exp mx1 rh02842279 m1
Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , <t>Mx1</t> , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.
Gene Exp Mx1 Rh02842279 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , Mx1 , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.

Journal: The Journal of Experimental Medicine

Article Title: Role for NF-κB in herpes encephalitis pathology in mice genocopying an inborn error of IRF3-IFN immunity

doi: 10.1084/jem.20250064

Figure Lengend Snippet: Elevated proinflammatory cytokine levels in the brain of Irf3 R278Q/R278Q mice upon HSV-1 infection. (A–F) Expression of Ifnb , Mx1 , Tnfa , Il1b , Il6 , and Ccl2 in brain stems from WT or Irf3 R278Q/R278Q mice on days 1–4 after infection, measured by RT-qPCR. UI, uninfected control. WT, n = 5–7; Irf3 R278Q/R278Q , n = 5–12. (G–J) Mesoscale analysis of cytokine levels (TNFα, CCL2, and IFNγ) (G–I) and HSV-1 titer in brain stem homogenates on day 5 after infection quantified by plaque assay (J) (WT UI, n = 4, WT, n = 9; Irf3 R278Q/R278Q UI, n = 4; Irf3 R278Q/R278Q , n = 8). (K) Expression of Tnfa in brain stems from WT ( n = 7), Irf3 −/− ( n = 5), Irf3 R278Q/R278Q ( n = 9), and Irf3 WT/R278Q ( n = 6) mice on day 5 after HSV-1 infection, measured by RT-qPCR. (L–N) Ifnb, Tnfa , and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with 0.5 μM PLX5622 (PLX) for microglia depletion. (O and P) Tnfa and Il6 response 16 h after infection with 1.0 MOI HSV-1 in MBCs treated with NF-κB inhibitors BMS-345541 (2 μM), PDTC (25 μM), or saline. UI controls were included. (Q and S) Ifnb and Tnfa mRNA levels in murine microglia from WT, Irf3 WT/R278Q , and Irf3 R278Q/R278Q mice 24 h after HSV-1 infection at increasing virus MOI as indicated. (R and T) IFNB1 and TNFA mRNA levels in iPSC-derived microglia from the IRF3 WT/R285Q HSE patient and controls 24 h after HSV-1 infection at increasing virus MOI as indicated. Expression data were normalized to β-actin and shown as fold change compared with the UI control. All in vitro experiments were performed in triplicates and independently repeated at least three times. Cytokine expression kinetics were compared between the groups using a mixed-effects analysis with Geisser-Greenhouse correction for multiple interacting variables (time and genotype) (A–F), error bars; SEM. Statistical analyses of cytokine and virus levels in brain stem homogenates (G–J and L–T) were analyzed by two-tailed two-way ANOVA for difference of means, followed by an unpaired t test of means, error bars; SD. CNS cell experiments (K) were analyzed with a two-tailed one-way ANOVA for difference of means followed by an unpaired t test of means. P values <0.05 were considered statistically significant, *P < 0.05, **P < 0.01, and ***P < 0.001. UT, untreated; MOI, multiplicity of infection.

Article Snippet: Quantitative PCR was performed using the following TaqMan Gene Expression Assays (Applied Biosystems): ACTB (Hs01060665_g1), 18S (Hs03003631_g1), IFNB (Hs01077958_s1), IL6 (Hs00174131_m1), TNFA (Hs00174128_m1), IL1B (Hs01555410), MX1 (Hs00895598_m1), CXCL10 (Hs00171042), and ISG15 (Hs01921425). mRNA levels of interest were normalized to the housekeeping gene ACTB or 18S (as indicated) using the ΔΔCt method.

Techniques: Infection, Expressing, Quantitative RT-PCR, Control, Plaque Assay, Saline, Virus, Derivative Assay, In Vitro, Two Tailed Test