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brdu cell proliferation assay kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc brdu cell proliferation assay kit
    Brdu Cell Proliferation Assay Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/brdu+kit/us12599592-908-13-19
    Average 86 stars, based on 1 article reviews
    brdu cell proliferation assay kit - by Bioz Stars, 2026-10
    86/100 stars

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    Related Articles

    BrdU Staining:

    Article Title: Identification of a Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype
    Article Snippet: The images were analyzed using ImageJ software. . BrdU assay Cells were plated in 96-well plate in growth medium and were treated for the duration indicated. .. BrdU assay was performed on cells using Cell Signaling BrdU kit (Danvers, MA). . Gene expression assay Cells were plated in 96 well plates in charcoal stripped serum-containing medium and maintained for two days. ..

    Article Title: Identification of a targetable JAK-STAT enriched androgen receptor and androgen receptor splice variant positive triple-negative breast cancer subtype.
    Article Snippet: .. BrdU assay was performed on cells using Cell Signaling BrdU kit (Danvers, MA). ..

    Gene Expression:

    Article Title: Identification of a Targetable JAK-STAT Enriched Androgen Receptor (AR) and AR Splice Variant Positive Triple Negative Breast Cancer Subtype
    Article Snippet: The images were analyzed using ImageJ software. . BrdU assay Cells were plated in 96-well plate in growth medium and were treated for the duration indicated. .. BrdU assay was performed on cells using Cell Signaling BrdU kit (Danvers, MA). . Gene expression assay Cells were plated in 96 well plates in charcoal stripped serum-containing medium and maintained for two days. ..

    Suspension:

    Article Title: RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells
    Article Snippet: Analyses were initially performed using the kits marketed by Roche (Mannheim, Germany; #114446141001 or #11647229001) and continued using the BrdU Cell Proliferation Assay Kit marketed by Cell Signaling (Danvers, MA, USA, #6813S). .. Due to the suspension of deliveries, another BrdU kit (BrdU Cell Proliferation Assay Kit, #6813, Cell Signaling) had to be implemented into the study at later stages. ..

    BrdU Cell Proliferation Assay:

    Article Title: RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells
    Article Snippet: Analyses were initially performed using the kits marketed by Roche (Mannheim, Germany; #114446141001 or #11647229001) and continued using the BrdU Cell Proliferation Assay Kit marketed by Cell Signaling (Danvers, MA, USA, #6813S). .. Due to the suspension of deliveries, another BrdU kit (BrdU Cell Proliferation Assay Kit, #6813, Cell Signaling) had to be implemented into the study at later stages. ..



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    Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) <t>Cell</t> <t>proliferation</t> detected by bromodeoxyuridine <t>(BrdU)</t> staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).
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    Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine <t>(BrdU)</t> staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).
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    Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine <t>(BrdU)</t> staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).
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    Image Search Results


    Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine (BrdU) staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).

    Journal: Cell Reports Medicine

    Article Title: Macrophage-mimetic photothermal nanotherapeutics regulate mitochondrial homeostasis and inflammatory cascades in lung ischemia-reperfusion injury

    doi: 10.1016/j.xcrm.2026.102768

    Figure Lengend Snippet: Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine (BrdU) staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).

    Article Snippet: Cell proliferation was assessed using BrdU kits ( GC310002 , Servicebio) and Cell Counting Kit-8 (CCK-8) assays (C0041, Beyotime) per manufacturer protocols.

    Techniques: Labeling, Adsorption, Incubation, Centrifugation, Cell Counting, CCK-8 Assay, Irradiation, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Gene Expression, Immunofluorescence, Expressing, Staining, BrdU Staining, Flow Cytometry, Control

    Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine (BrdU) staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).

    Journal: Cell Reports Medicine

    Article Title: Macrophage-mimetic photothermal nanotherapeutics regulate mitochondrial homeostasis and inflammatory cascades in lung ischemia-reperfusion injury

    doi: 10.1016/j.xcrm.2026.102768

    Figure Lengend Snippet: Targeted repair of hypoxia/reoxygenation (H/R)-injured lung epithelial cells by Rg3@PACVs (A) Cellular uptake of Dio-labeled Rg3@PACVs (green) by H/R-injured BEAS-2B cells. Fluorescent localization was analyzed with or without pretreatment of endocytosis inhibitors (filipin, chlorpromazine, or chloroquine) (scale bars, 20 μm). (B–E) Cytokine adsorption capacity assessed by co-incubation of Rg3@PACVs (500 or 250 μg/mL) with inflammatory cytokines (IL-6, TNF-α, IL-1β, and CCL-2). Cytokine concentrations in supernatants were measured after centrifugation ( ∗∗∗ p < 0.001 vs. 0 μg/mL; # p < 0.05, ## p < 0.01 vs. 250 μg/mL; n = 3 biological replicates). (F) Cell viability of H/R-treated BEAS-2B cells assessed by cell counting kit-8 (CCK-8) assay. Cells were treated with Rg3, PACVs, or Rg3@PACVs with or without near-infrared (NIR) irradiation. (G–I) Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of inflammatory gene expression (IL-6, IL-1β, and TNF-α) in H/R-stimulated BEAS-2B cells under different pretreatment conditions. (J) Immunofluorescence showing expression and co-localization of NLRP3 (green) and COX2 (red) in H/R-injured lung epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 100 μm. (K) Cell proliferation detected by bromodeoxyuridine (BrdU) staining (red) in the above epithelial cells. Nuclei stained with DAPI (blue). Scale bars, 50 μm. (L) Apoptosis ratio analyzed by flow cytometry using Annexin V-Allophycocyanin (Annexin V-APC) and 7-Aminoactinomycin D (7-AAD) staining. Data are presented as the mean ± SD and analyzed using one-way ANOVA (B–E and G–I) and two-way ANOVA (F) with Tukey’s post hoc test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. H/R; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. H/R + Rg3@PACVs; n = 3 biological replicates, for F–I).

    Article Snippet: BrdU ELISA kit , Servicebio , Cat# GC310002.

    Techniques: Labeling, Adsorption, Incubation, Centrifugation, Cell Counting, CCK-8 Assay, Irradiation, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Gene Expression, Immunofluorescence, Expressing, Staining, BrdU Staining, Flow Cytometry, Control