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hsv 60  (InvivoGen)


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    Structured Review

    InvivoGen hsv 60
    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
    Hsv 60, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 45 article reviews
    hsv 60 - by Bioz Stars, 2026-05
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    1) Product Images from "Caspase-mediated DDX46 cleavage unchains antiviral immunity"

    Article Title: Caspase-mediated DDX46 cleavage unchains antiviral immunity

    Journal: mBio

    doi: 10.1128/mbio.03519-25

    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or HSV-60, panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
    Figure Legend Snippet: Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or HSV-60, panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.

    Techniques Used: Virus, Infection, Control, Transfection, Plasmid Preparation



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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or <t>HSV-60,</t> panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.
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    Image Search Results


    Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or HSV-60, panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.

    Journal: mBio

    Article Title: Caspase-mediated DDX46 cleavage unchains antiviral immunity

    doi: 10.1128/mbio.03519-25

    Figure Lengend Snippet: Virus infection or treatment with RNA ligands induces reduced DDX46 protein levels. ( A–C ) HeLa cells were mock-infected or infected with VSV ( A ), NDV ( B ), or HSV-1 ( C ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of VSV-G, NDV-NP, or HSV-1-gD were analyzed by WB. β-Actin served as the loading control. ( D–F ) Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the VSV ( D ), NDV ( E ), and HSV-1 ( F ) infection groups. ( G–J ) HeLa cells were transfected with RNA ligands [poly(I:C) or 3p-hpRNA, panels G and H ] or DNA ligands [poly(G:C) or HSV-60, panels I and J ] for 18 h. Protein levels of DDX46 were analyzed by WB. β-Actin served as the loading control. Representative results, with graphs representing the band intensity ratios of DDX46/β-actin normalized to the control conditions for the RNA ligands ( H ) or DNA ligand treatment groups ( J ). ( K ) Schematic diagram of DDX46 isoform I (full-length; DDX46-I) and isoform II (lacking valine at amino acid 872; DDX46-II). ( L–N ) HeLa cells were transfected with the empty vector p3×Flag, Flag-DDX46-I, or Flag-DDX46-II for 24 h, then mock infected or infected with VSV ( L ), NDV ( M ), or HSV-1 ( N ) at an MOI of 1 for 6, 12, 18, and 24 h. Protein levels of exogenous Flag-DDX46 and viral proteins (VSV-G, NDV-NP, or HSV-1-gD) were analyzed by WB. β-Actin served as the loading control. Data are presented as means from three independent experiments. *** P < 0.001.

    Article Snippet: Autophagy inhibitors wortmannin (W1628, Sigma-Aldrich) and chloroquine (CQ) (C6628, Sigma-Aldrich) were utilized at concentrations of 300 nM and 25 μM, respectively. poly(I:C) (tlrl-pic), 3p-hpRNA (tlrl-hprna), HSV-60 (tlrl-hsv60n), and poly(G:C) (tlrl-pgcn) were all obtained from Invivogen.

    Techniques: Virus, Infection, Control, Transfection, Plasmid Preparation