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mouse anti human cdk9 mab  (Novus Biologicals)


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    Novus Biologicals mouse anti human cdk9 mab
    a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of <t>CDK9</t> mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.
    Mouse Anti Human Cdk9 Mab, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+human+cdk9+mab/Mouse+anti-Human+IgG2+Fc+Secondary+Antibody+(3C7)/pmc07449975-146-19-23
    Average 90 stars, based on 5 article reviews
    mouse anti human cdk9 mab - by Bioz Stars, 2026-09
    90/100 stars

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    1) Product Images from "ASF1B promotes cervical cancer progression through stabilization of CDK9"

    Article Title: ASF1B promotes cervical cancer progression through stabilization of CDK9

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-020-02872-5

    a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of CDK9 mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.
    Figure Legend Snippet: a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of CDK9 mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.

    Techniques Used: Western Blot, SDS Page, Expressing, shRNA, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Control, Two Tailed Test, Staining, Imaging, Fluorescence

    The results of proteome analysis.
    Figure Legend Snippet: The results of proteome analysis.

    Techniques Used: Functional Assay

    Related Articles

    Incubation:

    Article Title: ASF1B promotes cervical cancer progression through stabilization of CDK9
    Article Snippet: .. The cells were then incubated with primary antibodies (1:100), including rabbit anti-human ASF1B mAb (Cell Signaling, Danvers, MA) and mouse anti-human CDK9 mAb (Novus Biologicals, Colorado, USA) at 4 °C overnight. .. The cells were washed with PBS and then incubated with the appropriate Alexa-488- or TRITC-conjugated secondary antibodies (1:200; Proteintech, Chicago, USA) at room temperature for 60 min.



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    Novus Biologicals mouse anti human cdk9 mab
    a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of <t>CDK9</t> mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.
    Mouse Anti Human Cdk9 Mab, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+human+cdk9+mab/Mouse+anti-Human+IgG2+Fc+Secondary+Antibody+(3C7)/pmc07449975-146-19-23
    Average 90 stars, based on 1 article reviews
    mouse anti human cdk9 mab - by Bioz Stars, 2026-09
    90/100 stars
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    a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of CDK9 mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.

    Journal: Cell Death & Disease

    Article Title: ASF1B promotes cervical cancer progression through stabilization of CDK9

    doi: 10.1038/s41419-020-02872-5

    Figure Lengend Snippet: a Western blots were performed to confirm the IP efficiency. b SDS-PAGE was conducted to analyze the production of IP. c Levels of CDK9 mRNA expression in stable ASF1B-shRNA HeLa cells. d. Protein expression of CDK9 in stable ASF1B-shRNA HeLa cells. e. Co-IP was performed to detect CDK9-ASF1B using anti-ASF1B beads and anti-CDK9 beads. f ASF1B-shRNA-HeLa cells or scrambled cells were treated with CHX at 20 μg/ml for 0, 4, 8, 12, and 16 h, and then the CDK9 expression level was determined by western blot. g ASF1B mediates stabilization through the ubiquitin proteasome pathway. ASF1B-shRNA HeLa cells or control cells were treated with proteasome inhibitor MG132 at 5 μM for 4 h, and then the CDK9 expression level was examined by western blot. h Quantification of the results in ( d ). Data are mean ± SEM, n = 3, and two-tailed unpaired Student’s t test was used. *** p < 0.001. i Colocalization of ASF1B and CDK9 in the nucleus. Immunofluorescent staining and imaging were used to visualize the colocalization of ASF1B (green fluorescence) and CDK9 (red fluorescence) in stable ASF1B-shRNA HeLa cells and corresponding scrambled cells. j A schematic model of this work. A schematic diagram showing the signaling pathway of the ASF1B-mediated effect on cervical cancer cell growth via the ASF1B/CDK9 axis.

    Article Snippet: The cells were then incubated with primary antibodies (1:100), including rabbit anti-human ASF1B mAb (Cell Signaling, Danvers, MA) and mouse anti-human CDK9 mAb (Novus Biologicals, Colorado, USA) at 4 °C overnight.

    Techniques: Western Blot, SDS Page, Expressing, shRNA, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Control, Two Tailed Test, Staining, Imaging, Fluorescence

    The results of proteome analysis.

    Journal: Cell Death & Disease

    Article Title: ASF1B promotes cervical cancer progression through stabilization of CDK9

    doi: 10.1038/s41419-020-02872-5

    Figure Lengend Snippet: The results of proteome analysis.

    Article Snippet: The cells were then incubated with primary antibodies (1:100), including rabbit anti-human ASF1B mAb (Cell Signaling, Danvers, MA) and mouse anti-human CDK9 mAb (Novus Biologicals, Colorado, USA) at 4 °C overnight.

    Techniques: Functional Assay