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null adenovirus  (Vector Biolabs)


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    Structured Review

    Vector Biolabs null adenovirus
    A) AML12 cells transduced with ATGL or GFP control <t>adenoviruses</t> were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed
    Null Adenovirus, supplied by Vector Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 133 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/null adenovirus/product/Vector Biolabs
    Average 96 stars, based on 133 article reviews
    null adenovirus - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "ATGL-catalyzed lipid catabolism promotes DNA repair"

    Article Title: ATGL-catalyzed lipid catabolism promotes DNA repair

    Journal: bioRxiv

    doi: 10.64898/2026.04.03.716381

    A) AML12 cells transduced with ATGL or GFP control adenoviruses were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed
    Figure Legend Snippet: A) AML12 cells transduced with ATGL or GFP control adenoviruses were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed

    Techniques Used: Transduction, Control, Irradiation, Isolation, Knock-In, Incubation, Immunofluorescence, Western Blot, Single Cell Gel Electrophoresis, Software



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    A) AML12 cells transduced with ATGL or GFP control <t>adenoviruses</t> were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed
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    Image Search Results


    A) AML12 cells transduced with ATGL or GFP control adenoviruses were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed

    Journal: bioRxiv

    Article Title: ATGL-catalyzed lipid catabolism promotes DNA repair

    doi: 10.64898/2026.04.03.716381

    Figure Lengend Snippet: A) AML12 cells transduced with ATGL or GFP control adenoviruses were treated with 30 μM etoposide for the indicated times and assayed for γH2Ax. B) Quantification of A. *p<0.05, **p<0.01. C) AML12 cells transduced with ATGL or GFP control adenoviruses were irradiated (10 Gy) and harvested at the indicated times post-IR. D) Quantification of C. **p<0.01. E) Primary MEFs were isolated from WT or ATGL knock-in (AKI) mice, followed by etoposide incubation for 6 hours. Immunofluorescence was performed for γH2Ax, and cells were imaged using the Agilent Gen5 Cytation. Representative γH2Ax images and foci distribution are shown. F) Cells were treated with DGAT inhibitors for 24 hours, followed by ATGL adenoviral transduction, followed by 24 hours of etoposide treatment. Western blotting for γH2Ax, β-actin, and ATGL. G) AML12 cells were treated as in F. The Comet assay was performed on cells after 24 hours of etoposide. Comets were quantified with OpenComet software. A minimum of 180 comets were quantified per condition. Statistics: one-way ANOVA with Tukey’s post hoc test. ****p<0.0001. H) γH2Ax results and quantification from tissues harvested from E2A Cre-ATGL (AKI) mice irradiated with 7.5 Gy + 4-hour recovery. Mice were of mixed sexes, n=4 mice. P-values from one-way ANOVA are displayed

    Article Snippet: For adenoviral transductions, ATGL (Lot: 20160819, mouse ATGL) was obtained from VectorBiolabs, TrackGFP (adGFP) was obtained from UNC Gene Therapy Center, and Null adenovirus was obtained from VectorBiolabs (#1300).

    Techniques: Transduction, Control, Irradiation, Isolation, Knock-In, Incubation, Immunofluorescence, Western Blot, Single Cell Gel Electrophoresis, Software

    CFTR overexpression promotes skeletal muscle function in aged mice. (A, B) qPCR for myogenesis/atrophy‐ (A) and autophagy‐ (B) related genes in gastrocnemii collected from 15‐month‐old female wild‐type mice at week 1 (W1) or week 2 (W2) after injected with adenoviruses containing human CFTR gene (Adv‐CFTR) or control viruses (Adv‐Ctrl). *** p < 0.001, Two‐way ANOVA with Bonferroni's multiple comparison test n = 4. (C, D) Western blot for CFTR, MYOG, and LC3‐ β (C), and muscle functional tests of sF t , sF 0 and force loss (D, see methods) in gastrocnemii collected at W2. * p < 0.05, ** p < 0.01, unpaired t‐test n = 4 (C) and 5 (D). (E) DEXA measurement of lean mass of the lower hindlimb injected with Adv‐CFTR or Adv‐Ctrl at W1 or W2. ** p < 0.01, Two‐way ANOVA with Bonferroni's multiple comparison test n = 3–4. (F) Representative images of MHC and myosin ATPase staining with quantification of slow‐ or fast‐ twitch fibres in the Adv‐CFTR‐ or Adv‐Ctrl‐treated gastrocnemii collected at W2. ** p < 0.01, unpaired t‐test n = 4. Scale bars, 20 μm.

    Journal: Journal of Cachexia, Sarcopenia and Muscle

    Article Title: Defective Cystic Fibrosis Transmembrane Conductance Regulator Accelerates Skeletal Muscle Aging by Impairing Autophagy/Myogenesis

    doi: 10.1002/jcsm.13708

    Figure Lengend Snippet: CFTR overexpression promotes skeletal muscle function in aged mice. (A, B) qPCR for myogenesis/atrophy‐ (A) and autophagy‐ (B) related genes in gastrocnemii collected from 15‐month‐old female wild‐type mice at week 1 (W1) or week 2 (W2) after injected with adenoviruses containing human CFTR gene (Adv‐CFTR) or control viruses (Adv‐Ctrl). *** p < 0.001, Two‐way ANOVA with Bonferroni's multiple comparison test n = 4. (C, D) Western blot for CFTR, MYOG, and LC3‐ β (C), and muscle functional tests of sF t , sF 0 and force loss (D, see methods) in gastrocnemii collected at W2. * p < 0.05, ** p < 0.01, unpaired t‐test n = 4 (C) and 5 (D). (E) DEXA measurement of lean mass of the lower hindlimb injected with Adv‐CFTR or Adv‐Ctrl at W1 or W2. ** p < 0.01, Two‐way ANOVA with Bonferroni's multiple comparison test n = 3–4. (F) Representative images of MHC and myosin ATPase staining with quantification of slow‐ or fast‐ twitch fibres in the Adv‐CFTR‐ or Adv‐Ctrl‐treated gastrocnemii collected at W2. ** p < 0.01, unpaired t‐test n = 4. Scale bars, 20 μm.

    Article Snippet: Adenovirus‐packaged CFTR (Adv‐CFTR, pAdeno‐MCMV‐CFTR‐T2A‐3Flag‐T2AmCherry) or null sequence (Adv‐vector, pAdeno‐MCMV‐3Flag‐T2A‐mCherry) purchased from OBiO Technology (Shanghai) was used.

    Techniques: Over Expression, Injection, Control, Comparison, Western Blot, Functional Assay, Staining