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fnar1 inhibitor  (MedChemExpress)


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    MedChemExpress fnar1 inhibitor
    EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN <t>alpha‐IFNAR‐IN‐1)</t> for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.
    Fnar1 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fnar1+inhibitor/pmc12955960-240-50-59?v=MedChemExpress
    Average 94 stars, based on 28 article reviews
    fnar1 inhibitor - by Bioz Stars, 2026-07
    94/100 stars

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    1) Product Images from "EGR Proteins Mediate Interferon‐Independent Anti‐HSV‐1 Responses Through Viral and Host Targets"

    Article Title: EGR Proteins Mediate Interferon‐Independent Anti‐HSV‐1 Responses Through Viral and Host Targets

    Journal: Advanced Science

    doi: 10.1002/advs.202515546

    EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN alpha‐IFNAR‐IN‐1) for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.
    Figure Legend Snippet: EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN alpha‐IFNAR‐IN‐1) for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.

    Techniques Used: Expressing, Transfection, Infection, Virus, Titration, Western Blot, Quantitative RT-PCR, Plasmid Preparation, Luciferase, Two Tailed Test



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    fnar1 inhibitor  (MedChemExpress)
    94
    MedChemExpress fnar1 inhibitor
    EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN <t>alpha‐IFNAR‐IN‐1)</t> for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.
    Fnar1 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fnar1+inhibitor/pmc12955960-240-50-59?v=MedChemExpress
    Average 94 stars, based on 1 article reviews
    fnar1 inhibitor - by Bioz Stars, 2026-07
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN alpha‐IFNAR‐IN‐1) for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.

    Journal: Advanced Science

    Article Title: EGR Proteins Mediate Interferon‐Independent Anti‐HSV‐1 Responses Through Viral and Host Targets

    doi: 10.1002/advs.202515546

    Figure Lengend Snippet: EGR1 suppresses HSV‐1 replication by enhancing IRF7 expression. (A) Neuro‐2a cells were transfected with the indicated siRNAs for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (B) Left, Neuro‐2a cells were transfected with the indicated siRNAs for 18 h, then transfected with the indicated plasmids for 20 h, then infected with HSV‐1 (MOI = 0.2) for 44 h before virus titration. Right, Neuro‐2a cells were transfected with the indicated siRNAs for 16 h, then transfected with the indicated plasmids for 22 h, then infected with HSV‐1 (MOI = 0.5) for 24 h before virus titration. (C) Left, Neuro‐2a cells were transfected with 400 ng/mL of indicated plasmids expressing flag‐tagged proteins for 24 h before Western blot analysis using a flag antibody. Right, Neuro‐2a cells were transfected with the indicated plasmids for 24 h, then infected with HSV‐1 (MOI = 0.2) for 48 h before virus titration. (D) RT‐qPCR analysis of IRF7 mRNA at the indicted times after HSV‐1 infection of Neuro‐2a cells (MOI = 10). (E) N2A‐EGR1‐KO1 cells were co‐transfected with 300 ng/mL of pcDNA or pIRF7, 100 ng/mL of the ISRE‐luc plasmid and 50 ng/mL of the RL‐CMV plasmid for 24 h before luciferase assays. (F) N2A‐EGR1‐KO1 cells were untreated or pretreated with IFN‐α (500 IU/mL) for 12 h, then co‐transfected with 300 ng/mL of pcDNA or pEGR1, 100 ng/mL of ISRE‐luc, 50 ng/mL of RL‐CMV in the absence (left) or presence (right) of IFN‐α for 24 h before luciferase assays. (G) Neuro‐2a cells were transfected with the indicated plasmids for 22 h, then treated with DMSO or 2 µM IFNAR1 inhibitor (IFN alpha‐IFNAR‐IN‐1) for 16 h, and then infected with HSV‐1 (MOI = 0.2) in the presence of DMSO or the inhibitor for 40 h before virus titration. n = 3 biologically independent samples for all panels. Data were analyzed by one‐way ANOVA with Dunnett's multiple comparisons tests (A, C, D) or two‐way ANOVA with Sidak's multiple comparisons tests (B, G), two‐tailed unpaired t tests (E, F) and are presented as mean ± SD.

    Article Snippet: The following inhibitors were used at the following final concentrations: PDK1 inhibitor (BX‐795, 1 μ m , MedChemExpress), PI3K inhibitor (PI‐103, 500 n m , MedChemExpress), MEK1/2 inhibitor (Binimetinib, 1 μ m , MedChemExpress), AKT inhibitor (MK‐2206, 1.25 μ m , MedChemExpress), ATM inhibitor (KU‐55933, 20 μ m , MedChemExpress), FNAR1 inhibitor (IFN alpha‐IFNAR‐IN‐1, HY‐12836A, 2 μ m , MedChemExpress), and JNK inhibitor (SP600125, 10 μ m , MedChemExpress).

    Techniques: Expressing, Transfection, Infection, Virus, Titration, Western Blot, Quantitative RT-PCR, Plasmid Preparation, Luciferase, Two Tailed Test