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polyclonal abs against gapdh and pcna antibody  (ImmunoWay Biotechnology Company)

 
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    ImmunoWay Biotechnology Company polyclonal abs against gapdh and pcna antibody
    Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for <t>PCNA</t> protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 <t>h.</t> <t>GAPDH</t> was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.
    Polyclonal Abs Against Gapdh And Pcna Antibody, supplied by ImmunoWay Biotechnology Company, 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/polyclonal+abs+against+gapdh+and+pcna+antibody/polyclonal+abs+against+gapdh+and+pcna+antibody/pmc06949814-76-24-25
    Average 90 stars, based on 1 article reviews
    polyclonal abs against gapdh and pcna antibody - by Bioz Stars, 2026-09
    90/100 stars

    Images

    1) Product Images from "High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways"

    Article Title: High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways

    Journal: International Journal of Clinical and Experimental Pathology

    doi:

    Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for PCNA protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 h. GAPDH was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.
    Figure Legend Snippet: Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for PCNA protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 h. GAPDH was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.

    Techniques Used: Western Blot, Control, CCK-8 Assay, Staining

    The effects of related receptors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were pretreated with Cu-CPT22 (50 nM), CLI-095 (1 ug/ml) and FPS-ZMI (230 nM) for 1 hour, followed by stimulation with HMGB1 1000 ng/ml for 48 h. A. Cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.
    Figure Legend Snippet: The effects of related receptors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were pretreated with Cu-CPT22 (50 nM), CLI-095 (1 ug/ml) and FPS-ZMI (230 nM) for 1 hour, followed by stimulation with HMGB1 1000 ng/ml for 48 h. A. Cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Techniques Used: CCK-8 Assay, Expressing, Western Blot, Control

    Effects of specific signaling pathway inhibitors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were incubated for 1 h with or without the protein kinase inhibitors BAY11-7082 (10 µM), U0126 (10 µM), SB203580 (10 µM) or SP600125 (50 µM) before stimulation with HMGB1 (1,000 ng/ml) for 48 h. A. The cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.
    Figure Legend Snippet: Effects of specific signaling pathway inhibitors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were incubated for 1 h with or without the protein kinase inhibitors BAY11-7082 (10 µM), U0126 (10 µM), SB203580 (10 µM) or SP600125 (50 µM) before stimulation with HMGB1 (1,000 ng/ml) for 48 h. A. The cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Techniques Used: Incubation, CCK-8 Assay, Expressing, Western Blot, Control

    Related Articles

    Incubation:

    Article Title: High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways
    Article Snippet: Whole-cell lysates (50 μg) were separated on a 10% SDS-PAGE and then transferred to nitrocellulose membranes (PALL, USA). .. After 60 min of incubation at room temperature in 5% non-fat milk in TBST, the membranes were exposed to polyclonal Abs against GAPDH and PCNA (Immunoway, USA), rabbit monoclonal Abs against Erk1/2 and phosphorylated Erk1/2 (Cell Signaling Biotechnology) and rabbit monoclonal Abs against phosphorylated p65 (Cell Signaling Biotechnology). .. IRDye 800 CW goat anti-rabbit IgG (H+L) (Licor, USA) was used as a secondary antibody.



    Similar Products

    polyclonal abs against gapdh and pcna antibody  (ImmunoWay Biotechnology Company)
    90
    ImmunoWay Biotechnology Company polyclonal abs against gapdh and pcna antibody
    Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for <t>PCNA</t> protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 <t>h.</t> <t>GAPDH</t> was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.
    Polyclonal Abs Against Gapdh And Pcna Antibody, supplied by ImmunoWay Biotechnology Company, 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/polyclonal+abs+against+gapdh+and+pcna+antibody/polyclonal+abs+against+gapdh+and+pcna+antibody/pmc06949814-76-24-25
    Average 90 stars, based on 1 article reviews
    polyclonal abs against gapdh and pcna antibody - by Bioz Stars, 2026-09
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for PCNA protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 h. GAPDH was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways

    doi:

    Figure Lengend Snippet: Effect of HMGB1 on proliferation of RASMCs. A. Representative western blot analysis for PCNA protein. The primary RASMCs were treated with the indicated concentrations of HMGB1 (100-1000 ng/ml) for 48 h. GAPDH was selected to normalize the PCNA level. *P < 0.05 vs. Control cells; #P < 0.05 vs the RASMCs treated with HMGB1 100 ng/ml. B. Effect of HMGB1 on RASMCs proliferation detected by the CCK-8 assay. The primary RASMCs were treated with HMGB1 for 48 h. *P < 0.05 vs. Control cells; #P < 0.05 vs. the RASMCs treated with HMGB1 100 ng/ml. C. The RASMCs were treated with HMGB1 1000 ng/ml for 0, 12, 24, 48 h. *: P < 0.05 vs. unstimulated cells at 0 h; #: P < 0.05 vs the RASMCs treated with HMGB1 for 12 h; &: P < 0.05 vs the RASMCs treated with HMGB1 for 24 h. D. Cell viability was detected by trypan blue staining. Data are expressed as mean ± SEM from four independent experiments.

    Article Snippet: After 60 min of incubation at room temperature in 5% non-fat milk in TBST, the membranes were exposed to polyclonal Abs against GAPDH and PCNA (Immunoway, USA), rabbit monoclonal Abs against Erk1/2 and phosphorylated Erk1/2 (Cell Signaling Biotechnology) and rabbit monoclonal Abs against phosphorylated p65 (Cell Signaling Biotechnology).

    Techniques: Western Blot, Control, CCK-8 Assay, Staining

    The effects of related receptors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were pretreated with Cu-CPT22 (50 nM), CLI-095 (1 ug/ml) and FPS-ZMI (230 nM) for 1 hour, followed by stimulation with HMGB1 1000 ng/ml for 48 h. A. Cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways

    doi:

    Figure Lengend Snippet: The effects of related receptors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were pretreated with Cu-CPT22 (50 nM), CLI-095 (1 ug/ml) and FPS-ZMI (230 nM) for 1 hour, followed by stimulation with HMGB1 1000 ng/ml for 48 h. A. Cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Article Snippet: After 60 min of incubation at room temperature in 5% non-fat milk in TBST, the membranes were exposed to polyclonal Abs against GAPDH and PCNA (Immunoway, USA), rabbit monoclonal Abs against Erk1/2 and phosphorylated Erk1/2 (Cell Signaling Biotechnology) and rabbit monoclonal Abs against phosphorylated p65 (Cell Signaling Biotechnology).

    Techniques: CCK-8 Assay, Expressing, Western Blot, Control

    Effects of specific signaling pathway inhibitors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were incubated for 1 h with or without the protein kinase inhibitors BAY11-7082 (10 µM), U0126 (10 µM), SB203580 (10 µM) or SP600125 (50 µM) before stimulation with HMGB1 (1,000 ng/ml) for 48 h. A. The cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF- κ B pathways

    doi:

    Figure Lengend Snippet: Effects of specific signaling pathway inhibitors on HMGB1-induced proliferation of RASMCs. The primary RASMCs were incubated for 1 h with or without the protein kinase inhibitors BAY11-7082 (10 µM), U0126 (10 µM), SB203580 (10 µM) or SP600125 (50 µM) before stimulation with HMGB1 (1,000 ng/ml) for 48 h. A. The cell proliferation was evaluated by a CCK-8 assay. B. The PCNA protein expression was determined by western blot and GAPDH was used as the internal control. *: P < 0.05 vs. unstimulated cells; #: P < 0.05 vs. the RASMCs treated with HMGB1. Data are expressed as mean ± SEM from four independent experiments.

    Article Snippet: After 60 min of incubation at room temperature in 5% non-fat milk in TBST, the membranes were exposed to polyclonal Abs against GAPDH and PCNA (Immunoway, USA), rabbit monoclonal Abs against Erk1/2 and phosphorylated Erk1/2 (Cell Signaling Biotechnology) and rabbit monoclonal Abs against phosphorylated p65 (Cell Signaling Biotechnology).

    Techniques: Incubation, CCK-8 Assay, Expressing, Western Blot, Control