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pcmv vsv g  (Addgene inc)


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    Addgene inc pcmv vsv g
    Pcmv Vsv G, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 2838 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits <t>VSV-G-mediated</t> entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
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    Identification of a heat-stable factor in human serum that competitively inhibits VSV-G-mediated entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

    Journal: Molecular Therapy Advances

    Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

    doi: 10.1016/j.omta.2026.201721

    Figure Lengend Snippet: Identification of a heat-stable factor in human serum that competitively inhibits VSV-G-mediated entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

    Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

    Techniques: Inhibition, Infection, Luciferase, Activity Assay, Microscopy, Standard Deviation

    Retargeted VSVs also escape competitive inhibition by serum from other pre-clinical animal models Parental K562 or K562-EGFR cells were infected with VSV-GFP containing a wild-type (WT) G (MOI = 0.1) or an EGFR-retargeted G (mEGF; MOI = 1) in the presence of medium alone or 25% HI serum from the indicated species. After 24 h, GFP-positive cells were quantitated. Values represent the number of GFP-positive cells (with SD) relative to the medium alone (in parental K562 cells for VSV-G-WT and in K562-EGFR cells for VSV-G-mEGF) ( n = 2 experimental replicates).

    Journal: Molecular Therapy Advances

    Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

    doi: 10.1016/j.omta.2026.201721

    Figure Lengend Snippet: Retargeted VSVs also escape competitive inhibition by serum from other pre-clinical animal models Parental K562 or K562-EGFR cells were infected with VSV-GFP containing a wild-type (WT) G (MOI = 0.1) or an EGFR-retargeted G (mEGF; MOI = 1) in the presence of medium alone or 25% HI serum from the indicated species. After 24 h, GFP-positive cells were quantitated. Values represent the number of GFP-positive cells (with SD) relative to the medium alone (in parental K562 cells for VSV-G-WT and in K562-EGFR cells for VSV-G-mEGF) ( n = 2 experimental replicates).

    Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

    Techniques: Inhibition, Infection

    Retargeted VSV-G-pseudotyped lentiviral vectors effectively transduce cells in the presence of serum lipoproteins Parental K562, K562-EGFR, or K562-cKit cells were transduced with LV-GFP containing wild-type (WT) G, EGFR-retargeted G (mEGF), or cKit-retargeted G (SCF), respectively, at 2.8 × 10 4 lentiviral particles/well, in the presence or absence of 60% heat-inactivated (HI) human serum. After 48 h, GFP-positive cells were imaged using a fluorescence microscope (A) and quantitated by Imaging Cytometry (B). Values represent the number of GFP-positive cells (with SD) relative to the medium alone for each LV ( n = 4 from 3 experimental replicates). A one-way ANOVA was performed on raw GFP + cell values comparing medium to serum for each LV. ns, not significant; ∗∗∗∗ p < 0.0001.

    Journal: Molecular Therapy Advances

    Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

    doi: 10.1016/j.omta.2026.201721

    Figure Lengend Snippet: Retargeted VSV-G-pseudotyped lentiviral vectors effectively transduce cells in the presence of serum lipoproteins Parental K562, K562-EGFR, or K562-cKit cells were transduced with LV-GFP containing wild-type (WT) G, EGFR-retargeted G (mEGF), or cKit-retargeted G (SCF), respectively, at 2.8 × 10 4 lentiviral particles/well, in the presence or absence of 60% heat-inactivated (HI) human serum. After 48 h, GFP-positive cells were imaged using a fluorescence microscope (A) and quantitated by Imaging Cytometry (B). Values represent the number of GFP-positive cells (with SD) relative to the medium alone for each LV ( n = 4 from 3 experimental replicates). A one-way ANOVA was performed on raw GFP + cell values comparing medium to serum for each LV. ns, not significant; ∗∗∗∗ p < 0.0001.

    Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

    Techniques: Transduction, Fluorescence, Microscopy, Imaging, Cytometry