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apoptotic analysis  (Vazyme Biotech Co)


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    Vazyme Biotech Co apoptotic analysis
    Validation of top screen hits via individual amino acid mutations. A) Veen diagram showing the number of overlapping phosphorylation sites targeted by A3A‐BE3 or ABE‐BE3 pool with that detected by mass spectrum analysis (identified or quantifiable). B) Veen diagram showing the number of overlapping phosphorylation sites targeted by significantly enriched gRNAs from A3A‐BE3 ( n = 268) or ABE‐BE3 ( n = 160) pool with that detected by mass spectrum analysis (identified or quantifiable) and targeted by total pools. Top enriched gRNA targeting phosphorylation sites overlapped with quantifiable phosphorylation sites are presented. C) Normalized quantification of protein peptides containing phosphorylation sites (all phosphorylation sites reported within top 20 hits from A3A‐BE3 or ABE‐BE3 pool) in total protein or phosphorylation protein analysis. Two replicates were presented for each treatment. Gray boxes indicate peptides not detected in spectrum analysis. Genes presented in top 10 (Figure ) are highlighted in blue. D) Hct116 cells were transfected with CBE or ABE tools and targeting gRNAs to establish single cell clones containing expected mutations. One, two, or three clones containing expected mutations to disrupt phosphorylation sites were subjected to <t>apoptotic</t> assays in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h.
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    Images

    1) Product Images from "Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR‐Mediated Base Editors"

    Article Title: Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR‐Mediated Base Editors

    Journal: Advanced Science

    doi: 10.1002/advs.202200717

    Validation of top screen hits via individual amino acid mutations. A) Veen diagram showing the number of overlapping phosphorylation sites targeted by A3A‐BE3 or ABE‐BE3 pool with that detected by mass spectrum analysis (identified or quantifiable). B) Veen diagram showing the number of overlapping phosphorylation sites targeted by significantly enriched gRNAs from A3A‐BE3 ( n = 268) or ABE‐BE3 ( n = 160) pool with that detected by mass spectrum analysis (identified or quantifiable) and targeted by total pools. Top enriched gRNA targeting phosphorylation sites overlapped with quantifiable phosphorylation sites are presented. C) Normalized quantification of protein peptides containing phosphorylation sites (all phosphorylation sites reported within top 20 hits from A3A‐BE3 or ABE‐BE3 pool) in total protein or phosphorylation protein analysis. Two replicates were presented for each treatment. Gray boxes indicate peptides not detected in spectrum analysis. Genes presented in top 10 (Figure ) are highlighted in blue. D) Hct116 cells were transfected with CBE or ABE tools and targeting gRNAs to establish single cell clones containing expected mutations. One, two, or three clones containing expected mutations to disrupt phosphorylation sites were subjected to apoptotic assays in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h.
    Figure Legend Snippet: Validation of top screen hits via individual amino acid mutations. A) Veen diagram showing the number of overlapping phosphorylation sites targeted by A3A‐BE3 or ABE‐BE3 pool with that detected by mass spectrum analysis (identified or quantifiable). B) Veen diagram showing the number of overlapping phosphorylation sites targeted by significantly enriched gRNAs from A3A‐BE3 ( n = 268) or ABE‐BE3 ( n = 160) pool with that detected by mass spectrum analysis (identified or quantifiable) and targeted by total pools. Top enriched gRNA targeting phosphorylation sites overlapped with quantifiable phosphorylation sites are presented. C) Normalized quantification of protein peptides containing phosphorylation sites (all phosphorylation sites reported within top 20 hits from A3A‐BE3 or ABE‐BE3 pool) in total protein or phosphorylation protein analysis. Two replicates were presented for each treatment. Gray boxes indicate peptides not detected in spectrum analysis. Genes presented in top 10 (Figure ) are highlighted in blue. D) Hct116 cells were transfected with CBE or ABE tools and targeting gRNAs to establish single cell clones containing expected mutations. One, two, or three clones containing expected mutations to disrupt phosphorylation sites were subjected to apoptotic assays in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h.

    Techniques Used: Transfection, Clone Assay

    RSK2 and TP53BP1 mediate 5‐FU‐induced transcriptomic alterations. A) RNA‐seq analysis of differentially expressed genes in control (Hct116) or RPS6KA3 mutant cells without or without 5‐FU (20 × 10 −6 m ) treatment. Five group of genes (G1‐G5) with different features were presented. Representative genes and GO analysis for G1, G2, G4, and G5 groups were presented (P values for GO terms were also presented). B) Relative expression (Rel. Exp.) of TP53 , ELF3 , GDF15 , IDH2 , CCNB1 , and CDKN2C was presented as FPKM in control (WT/Hct116) or RPS6KA3 mutant cells without or without 5‐FU treatment from RNA‐seq analysis. C) RNA‐seq analysis of differentially expressed genes (G1’‐G5’) in control (Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment. Representative genes and GO analysis for G1’, G2’, G4’, and G5’ groups were presented (P values for GO terms were also presented). D) WT/Hct116) or TP53BP1 mutant cells were subjected to apoptotic analysis in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h. E) Veen diagram showing the number of overlapping genes between G2 versus G2’ or G4 versus G4’. F) Relative expression (Rel. Exp.) of CDKN3 and CDKN2C was presented as FPKM in control (WT/Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment from RNA‐seq analysis.
    Figure Legend Snippet: RSK2 and TP53BP1 mediate 5‐FU‐induced transcriptomic alterations. A) RNA‐seq analysis of differentially expressed genes in control (Hct116) or RPS6KA3 mutant cells without or without 5‐FU (20 × 10 −6 m ) treatment. Five group of genes (G1‐G5) with different features were presented. Representative genes and GO analysis for G1, G2, G4, and G5 groups were presented (P values for GO terms were also presented). B) Relative expression (Rel. Exp.) of TP53 , ELF3 , GDF15 , IDH2 , CCNB1 , and CDKN2C was presented as FPKM in control (WT/Hct116) or RPS6KA3 mutant cells without or without 5‐FU treatment from RNA‐seq analysis. C) RNA‐seq analysis of differentially expressed genes (G1’‐G5’) in control (Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment. Representative genes and GO analysis for G1’, G2’, G4’, and G5’ groups were presented (P values for GO terms were also presented). D) WT/Hct116) or TP53BP1 mutant cells were subjected to apoptotic analysis in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h. E) Veen diagram showing the number of overlapping genes between G2 versus G2’ or G4 versus G4’. F) Relative expression (Rel. Exp.) of CDKN3 and CDKN2C was presented as FPKM in control (WT/Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment from RNA‐seq analysis.

    Techniques Used: RNA Sequencing Assay, Mutagenesis, Expressing

    RSK2 or PAK4 inhibitors enhancer 5‐FU‐induced cell growth inhibition and apoptosis in colorectal cancer cells. A) Top 20 screen hits were subjected to phosphorylation network analysis using an online tool ( http://phosphorylationnetworks.org ). Black circled genes were from screen hits, genes with pink background represent known kinases, and genes with green background represent classical downstream targets. B) The upper panel displays the phosphorylation sites and functional domains (NTD, NH2‐terminal kinase domain; CTD, C‐terminal domain) identified within RSK2 protein as well as their catalyzing kinases (PDK1, ERK, FGFR3). The upper panel showing the results from western blot analysis of total RSK2, phosphorylated RSK2 at Thr577 (p‐RSK2 T577), and GAPDH expression in mock or 5‐FU‐treated Hct116 cells (20 × 10 −6 m for 6, 12, 24, and 48 h). C,D) Relative cell growth rates of Hct116 cells treated with increasing concentrations of RSK2 inhibitor (RSK2i) or PAK4 inhibitor (PAK4i). E–H) Relative cell growth rates of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. I) Apoptotic analysis of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. Proportions of early (Annexin V + /PI – ) or late (Annexin V + /PI + ) apoptotic cells were presented. J) Apoptotic analysis of Hct116 cells expressing control vector or MAP3K2‐S153E. Cells were treated with 5‐FU (5 × 10 −6 m ) or 5‐FU and RSK2 inhibitor (10 × 10 −6 m ) combinations for 72 h, and the proportions of early and late apoptotic cells were determined. K) Wildtype or P53 knockout (P53 KO) Hct116 cells were treated with 5‐FU (5 × 10 −6 m ), RSK2 inhibitor (10 × 10 −6 m ), or their combinations. Apoptotic assays were performed at 48 h. Western blot analysis was conducted to detect the expression of P53 in wildtype and P53 KO cells.
    Figure Legend Snippet: RSK2 or PAK4 inhibitors enhancer 5‐FU‐induced cell growth inhibition and apoptosis in colorectal cancer cells. A) Top 20 screen hits were subjected to phosphorylation network analysis using an online tool ( http://phosphorylationnetworks.org ). Black circled genes were from screen hits, genes with pink background represent known kinases, and genes with green background represent classical downstream targets. B) The upper panel displays the phosphorylation sites and functional domains (NTD, NH2‐terminal kinase domain; CTD, C‐terminal domain) identified within RSK2 protein as well as their catalyzing kinases (PDK1, ERK, FGFR3). The upper panel showing the results from western blot analysis of total RSK2, phosphorylated RSK2 at Thr577 (p‐RSK2 T577), and GAPDH expression in mock or 5‐FU‐treated Hct116 cells (20 × 10 −6 m for 6, 12, 24, and 48 h). C,D) Relative cell growth rates of Hct116 cells treated with increasing concentrations of RSK2 inhibitor (RSK2i) or PAK4 inhibitor (PAK4i). E–H) Relative cell growth rates of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. I) Apoptotic analysis of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. Proportions of early (Annexin V + /PI – ) or late (Annexin V + /PI + ) apoptotic cells were presented. J) Apoptotic analysis of Hct116 cells expressing control vector or MAP3K2‐S153E. Cells were treated with 5‐FU (5 × 10 −6 m ) or 5‐FU and RSK2 inhibitor (10 × 10 −6 m ) combinations for 72 h, and the proportions of early and late apoptotic cells were determined. K) Wildtype or P53 knockout (P53 KO) Hct116 cells were treated with 5‐FU (5 × 10 −6 m ), RSK2 inhibitor (10 × 10 −6 m ), or their combinations. Apoptotic assays were performed at 48 h. Western blot analysis was conducted to detect the expression of P53 in wildtype and P53 KO cells.

    Techniques Used: Inhibition, Functional Assay, Western Blot, Expressing, Plasmid Preparation, Knock-Out



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    Image Search Results


    Validation of top screen hits via individual amino acid mutations. A) Veen diagram showing the number of overlapping phosphorylation sites targeted by A3A‐BE3 or ABE‐BE3 pool with that detected by mass spectrum analysis (identified or quantifiable). B) Veen diagram showing the number of overlapping phosphorylation sites targeted by significantly enriched gRNAs from A3A‐BE3 ( n = 268) or ABE‐BE3 ( n = 160) pool with that detected by mass spectrum analysis (identified or quantifiable) and targeted by total pools. Top enriched gRNA targeting phosphorylation sites overlapped with quantifiable phosphorylation sites are presented. C) Normalized quantification of protein peptides containing phosphorylation sites (all phosphorylation sites reported within top 20 hits from A3A‐BE3 or ABE‐BE3 pool) in total protein or phosphorylation protein analysis. Two replicates were presented for each treatment. Gray boxes indicate peptides not detected in spectrum analysis. Genes presented in top 10 (Figure ) are highlighted in blue. D) Hct116 cells were transfected with CBE or ABE tools and targeting gRNAs to establish single cell clones containing expected mutations. One, two, or three clones containing expected mutations to disrupt phosphorylation sites were subjected to apoptotic assays in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h.

    Journal: Advanced Science

    Article Title: Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR‐Mediated Base Editors

    doi: 10.1002/advs.202200717

    Figure Lengend Snippet: Validation of top screen hits via individual amino acid mutations. A) Veen diagram showing the number of overlapping phosphorylation sites targeted by A3A‐BE3 or ABE‐BE3 pool with that detected by mass spectrum analysis (identified or quantifiable). B) Veen diagram showing the number of overlapping phosphorylation sites targeted by significantly enriched gRNAs from A3A‐BE3 ( n = 268) or ABE‐BE3 ( n = 160) pool with that detected by mass spectrum analysis (identified or quantifiable) and targeted by total pools. Top enriched gRNA targeting phosphorylation sites overlapped with quantifiable phosphorylation sites are presented. C) Normalized quantification of protein peptides containing phosphorylation sites (all phosphorylation sites reported within top 20 hits from A3A‐BE3 or ABE‐BE3 pool) in total protein or phosphorylation protein analysis. Two replicates were presented for each treatment. Gray boxes indicate peptides not detected in spectrum analysis. Genes presented in top 10 (Figure ) are highlighted in blue. D) Hct116 cells were transfected with CBE or ABE tools and targeting gRNAs to establish single cell clones containing expected mutations. One, two, or three clones containing expected mutations to disrupt phosphorylation sites were subjected to apoptotic assays in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h.

    Article Snippet: Cells treated with or without chemical reagents were stained with annexin V‐fluorescein isothiocyanate (FITC)/PI kit for apoptotic analysis (A211‐02; Vazyme, China).

    Techniques: Transfection, Clone Assay

    RSK2 and TP53BP1 mediate 5‐FU‐induced transcriptomic alterations. A) RNA‐seq analysis of differentially expressed genes in control (Hct116) or RPS6KA3 mutant cells without or without 5‐FU (20 × 10 −6 m ) treatment. Five group of genes (G1‐G5) with different features were presented. Representative genes and GO analysis for G1, G2, G4, and G5 groups were presented (P values for GO terms were also presented). B) Relative expression (Rel. Exp.) of TP53 , ELF3 , GDF15 , IDH2 , CCNB1 , and CDKN2C was presented as FPKM in control (WT/Hct116) or RPS6KA3 mutant cells without or without 5‐FU treatment from RNA‐seq analysis. C) RNA‐seq analysis of differentially expressed genes (G1’‐G5’) in control (Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment. Representative genes and GO analysis for G1’, G2’, G4’, and G5’ groups were presented (P values for GO terms were also presented). D) WT/Hct116) or TP53BP1 mutant cells were subjected to apoptotic analysis in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h. E) Veen diagram showing the number of overlapping genes between G2 versus G2’ or G4 versus G4’. F) Relative expression (Rel. Exp.) of CDKN3 and CDKN2C was presented as FPKM in control (WT/Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment from RNA‐seq analysis.

    Journal: Advanced Science

    Article Title: Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR‐Mediated Base Editors

    doi: 10.1002/advs.202200717

    Figure Lengend Snippet: RSK2 and TP53BP1 mediate 5‐FU‐induced transcriptomic alterations. A) RNA‐seq analysis of differentially expressed genes in control (Hct116) or RPS6KA3 mutant cells without or without 5‐FU (20 × 10 −6 m ) treatment. Five group of genes (G1‐G5) with different features were presented. Representative genes and GO analysis for G1, G2, G4, and G5 groups were presented (P values for GO terms were also presented). B) Relative expression (Rel. Exp.) of TP53 , ELF3 , GDF15 , IDH2 , CCNB1 , and CDKN2C was presented as FPKM in control (WT/Hct116) or RPS6KA3 mutant cells without or without 5‐FU treatment from RNA‐seq analysis. C) RNA‐seq analysis of differentially expressed genes (G1’‐G5’) in control (Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment. Representative genes and GO analysis for G1’, G2’, G4’, and G5’ groups were presented (P values for GO terms were also presented). D) WT/Hct116) or TP53BP1 mutant cells were subjected to apoptotic analysis in responding to 5‐FU (10 × 10 −6 or 20 × 10 −6 m ) treatment for 72 h. E) Veen diagram showing the number of overlapping genes between G2 versus G2’ or G4 versus G4’. F) Relative expression (Rel. Exp.) of CDKN3 and CDKN2C was presented as FPKM in control (WT/Hct116) or TP53BP1 mutant cells without or without 5‐FU treatment from RNA‐seq analysis.

    Article Snippet: Cells treated with or without chemical reagents were stained with annexin V‐fluorescein isothiocyanate (FITC)/PI kit for apoptotic analysis (A211‐02; Vazyme, China).

    Techniques: RNA Sequencing Assay, Mutagenesis, Expressing

    RSK2 or PAK4 inhibitors enhancer 5‐FU‐induced cell growth inhibition and apoptosis in colorectal cancer cells. A) Top 20 screen hits were subjected to phosphorylation network analysis using an online tool ( http://phosphorylationnetworks.org ). Black circled genes were from screen hits, genes with pink background represent known kinases, and genes with green background represent classical downstream targets. B) The upper panel displays the phosphorylation sites and functional domains (NTD, NH2‐terminal kinase domain; CTD, C‐terminal domain) identified within RSK2 protein as well as their catalyzing kinases (PDK1, ERK, FGFR3). The upper panel showing the results from western blot analysis of total RSK2, phosphorylated RSK2 at Thr577 (p‐RSK2 T577), and GAPDH expression in mock or 5‐FU‐treated Hct116 cells (20 × 10 −6 m for 6, 12, 24, and 48 h). C,D) Relative cell growth rates of Hct116 cells treated with increasing concentrations of RSK2 inhibitor (RSK2i) or PAK4 inhibitor (PAK4i). E–H) Relative cell growth rates of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. I) Apoptotic analysis of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. Proportions of early (Annexin V + /PI – ) or late (Annexin V + /PI + ) apoptotic cells were presented. J) Apoptotic analysis of Hct116 cells expressing control vector or MAP3K2‐S153E. Cells were treated with 5‐FU (5 × 10 −6 m ) or 5‐FU and RSK2 inhibitor (10 × 10 −6 m ) combinations for 72 h, and the proportions of early and late apoptotic cells were determined. K) Wildtype or P53 knockout (P53 KO) Hct116 cells were treated with 5‐FU (5 × 10 −6 m ), RSK2 inhibitor (10 × 10 −6 m ), or their combinations. Apoptotic assays were performed at 48 h. Western blot analysis was conducted to detect the expression of P53 in wildtype and P53 KO cells.

    Journal: Advanced Science

    Article Title: Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR‐Mediated Base Editors

    doi: 10.1002/advs.202200717

    Figure Lengend Snippet: RSK2 or PAK4 inhibitors enhancer 5‐FU‐induced cell growth inhibition and apoptosis in colorectal cancer cells. A) Top 20 screen hits were subjected to phosphorylation network analysis using an online tool ( http://phosphorylationnetworks.org ). Black circled genes were from screen hits, genes with pink background represent known kinases, and genes with green background represent classical downstream targets. B) The upper panel displays the phosphorylation sites and functional domains (NTD, NH2‐terminal kinase domain; CTD, C‐terminal domain) identified within RSK2 protein as well as their catalyzing kinases (PDK1, ERK, FGFR3). The upper panel showing the results from western blot analysis of total RSK2, phosphorylated RSK2 at Thr577 (p‐RSK2 T577), and GAPDH expression in mock or 5‐FU‐treated Hct116 cells (20 × 10 −6 m for 6, 12, 24, and 48 h). C,D) Relative cell growth rates of Hct116 cells treated with increasing concentrations of RSK2 inhibitor (RSK2i) or PAK4 inhibitor (PAK4i). E–H) Relative cell growth rates of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. I) Apoptotic analysis of Hct116 cells co‐treated with 5‐FU (2 × 10 −6 or 10 × 10 −6 m ) and RSK2i or PAK4i. Proportions of early (Annexin V + /PI – ) or late (Annexin V + /PI + ) apoptotic cells were presented. J) Apoptotic analysis of Hct116 cells expressing control vector or MAP3K2‐S153E. Cells were treated with 5‐FU (5 × 10 −6 m ) or 5‐FU and RSK2 inhibitor (10 × 10 −6 m ) combinations for 72 h, and the proportions of early and late apoptotic cells were determined. K) Wildtype or P53 knockout (P53 KO) Hct116 cells were treated with 5‐FU (5 × 10 −6 m ), RSK2 inhibitor (10 × 10 −6 m ), or their combinations. Apoptotic assays were performed at 48 h. Western blot analysis was conducted to detect the expression of P53 in wildtype and P53 KO cells.

    Article Snippet: Cells treated with or without chemical reagents were stained with annexin V‐fluorescein isothiocyanate (FITC)/PI kit for apoptotic analysis (A211‐02; Vazyme, China).

    Techniques: Inhibition, Functional Assay, Western Blot, Expressing, Plasmid Preparation, Knock-Out

    SAIF inhibited the growth of HUVEC cells. (A) Morphology of HUVEC cells after SAIF (12.5μΜ, 25μΜ, and 50μΜ) treatment. (B) Effect of SAIF (12.5μΜ, 25μΜ, and 50μΜ) on the viability of HUVEC cells. (C) Inhibitory effect of SAIF (25μΜ and 50μΜ) on clone formation of HUVEC cells. (D) Statistical histogram of HUVEC cell clones. (E) The apoptotic effect of SAIF on HUVEC cells was analyzed by Annexin V-FITC/PI staining. (F) SAIF treatment for 48 h altered the cell cycle distribution of HUVEC cells. Data are shown as mean ± SD, n = 3. *p < 0.05, **p < 0.01 and ***p < 0.001; one-way ANOVA followed by Dunnett's multiple comparison test.

    Journal: Heliyon

    Article Title: SAIF plays anti-angiogenesis via blocking VEGF-VEGFR2-ERK signal in tumor treatment

    doi: 10.1016/j.heliyon.2023.e18240

    Figure Lengend Snippet: SAIF inhibited the growth of HUVEC cells. (A) Morphology of HUVEC cells after SAIF (12.5μΜ, 25μΜ, and 50μΜ) treatment. (B) Effect of SAIF (12.5μΜ, 25μΜ, and 50μΜ) on the viability of HUVEC cells. (C) Inhibitory effect of SAIF (25μΜ and 50μΜ) on clone formation of HUVEC cells. (D) Statistical histogram of HUVEC cell clones. (E) The apoptotic effect of SAIF on HUVEC cells was analyzed by Annexin V-FITC/PI staining. (F) SAIF treatment for 48 h altered the cell cycle distribution of HUVEC cells. Data are shown as mean ± SD, n = 3. *p < 0.05, **p < 0.01 and ***p < 0.001; one-way ANOVA followed by Dunnett's multiple comparison test.

    Article Snippet: Finally, SAIF were diluted in 0.5% starvation medium, and added at the indicated concentration (0/12.5/25/50 μM) for 48 h. For the cell apoptosis assay, cells were stained using the Annexin V-FITC Apoptosis Analysis Kit (Cas:10-5 CE0 T, DOJINDO) and finally analyzed using the FACSAria™ flow cytometer (BD Biosciences).

    Techniques: Clone Assay, Staining

    The apoptotic effect in A549, MDA−MB 231, and SKOV3 cancerous cells after treatment with vehicle control and compounds 10 and 13 by annexin V−FITC/PI staining using flow cytometry. One-way ANOVA was used to test for statistical differences (* p < 0.05, ** p < 0.01).

    Journal: Molecules

    Article Title: Cell Cycle Arrest and Apoptosis-Inducing Ability of Benzimidazole Derivatives: Design, Synthesis, Docking, and Biological Evaluation

    doi: 10.3390/molecules27206899

    Figure Lengend Snippet: The apoptotic effect in A549, MDA−MB 231, and SKOV3 cancerous cells after treatment with vehicle control and compounds 10 and 13 by annexin V−FITC/PI staining using flow cytometry. One-way ANOVA was used to test for statistical differences (* p < 0.05, ** p < 0.01).

    Article Snippet: The assessment of apoptosis was performed using the Annexin V-FITC/PI analysis Kit, Cell Signaling Technology (CST), as instructed by the manufacturer [ ].

    Techniques: Staining, Flow Cytometry