vp 16  (Millipore)


Bioz Verified Symbol Millipore is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 85
    Name:
    Etoposide
    Description:
    Etoposide is synthesised from podophyllotoxins of plants
    Catalog Number:
    e1383
    Price:
    None
    Applications:
    Etoposide has been used:. to prepare drug stock solution in dimethyl sulfoxide (DMSO) and also to profile and compare the sensitivity of DT40 mutant cells. to incubate cells for cell viability assay . to treat neuro-2A cells to induce programmed cell death
    Buy from Supplier


    Structured Review

    Millipore vp 16
    Etoposide
    Etoposide is synthesised from podophyllotoxins of plants
    https://www.bioz.com/result/vp 16/product/Millipore
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    vp 16 - by Bioz Stars, 2020-09
    85/100 stars

    Images

    1) Product Images from "Calpain-mediated androgen receptor breakdown in apoptotic prostate cancer cells"

    Article Title: Calpain-mediated androgen receptor breakdown in apoptotic prostate cancer cells

    Journal:

    doi: 10.1002/jcp.21565

    Effect of VP-16 and celastrol on AR in intact cells and cell-free extracts
    Figure Legend Snippet: Effect of VP-16 and celastrol on AR in intact cells and cell-free extracts

    Techniques Used:

    Effect of various protease inhibitors on AR breakdown under cell-free conditions and in VP-16-treated intact cells
    Figure Legend Snippet: Effect of various protease inhibitors on AR breakdown under cell-free conditions and in VP-16-treated intact cells

    Techniques Used:

    2) Product Images from "The Iron Chelator Dp44mT Causes DNA Damage and Selective Inhibition of Topoisomerase IIα in Breast Cancer Cells"

    Article Title: The Iron Chelator Dp44mT Causes DNA Damage and Selective Inhibition of Topoisomerase IIα in Breast Cancer Cells

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-08-1437

    Topoisomerase IIα–mediated activity of Dp44mT. A, for topi activity, DNA corresponding to the 3′-end-labeled Pvu II/ Hind III fragment of pBluescript SK(−) phagemid DNA (pSK) was incubated with recombinant top1 in the absence of drug ( Top1 ) or in the presence of camptothecin, MJ-III-65, or increasing concentrations of Dp44mT (0.1–100 μmol/L). Reactions were carried out at 25°C for 20 min and stopped by addition of 0.5% SDS. To probe top2α-mediated cleavage activity of Dp44mT, the Pvu II/ Hin dIII fragment of pBluescript SK(−) phagemid DNA (pSK) was labeled at the 5′ ends, and reactions were carried out with recombinant top2α. VP-16 (100 μmol/L for 30 min) was included as a positive control. For testing top2β-mediated activity, recombinant top2β was used in the reactions as above with increasing concentrations of Dp44mT or with VP-16. B, apoptotic analysis of isogenic Nalm-6 leukemia cells (top2α/β +/+ , top2α +/− , and top2β −/− ) by propidium iodide staining and flow cytometry. The population of cells with sub-G 1 DNA content was compared at Dp44mT (0.1 μmol/L) or VP-16 (10 μmol/L) at 48 h. Representative of at least four independent experiments. The percentage of cells in each phase of cell cycle is provided. C, cellular topoisomerase cleavage complexes by top1, top2α, and top2β were determined using the immunocomplex of enzyme formation bioassay at 6 or 24 h as indicated in top2α/β wild-type Nalm-6 leukemic cells. Camptothecin (at 1 μmol/L) or VP-16 (at 100 μmol/L) was used as a positive control. Similar data were obtained in at least four independent experiments. D, Nalm-6 cells were also pretreated with pan-caspase inhibitor z-VAD-fmk (100 μmol/L for 30 min) and assayed for formation of nonapoptotic top2α cleavage complexes. E, Dp44mT sensitivity in siRNA-mediated top2α or top2β knockdown HeLa cells. Western blots indicate protein levels 48 h after siRNA transfection. Asterisks, statistically significant difference between the response in top2α +/− compared with top2α +/+ or top2β −/− cells. Bars, SD from two independent experiments.
    Figure Legend Snippet: Topoisomerase IIα–mediated activity of Dp44mT. A, for topi activity, DNA corresponding to the 3′-end-labeled Pvu II/ Hind III fragment of pBluescript SK(−) phagemid DNA (pSK) was incubated with recombinant top1 in the absence of drug ( Top1 ) or in the presence of camptothecin, MJ-III-65, or increasing concentrations of Dp44mT (0.1–100 μmol/L). Reactions were carried out at 25°C for 20 min and stopped by addition of 0.5% SDS. To probe top2α-mediated cleavage activity of Dp44mT, the Pvu II/ Hin dIII fragment of pBluescript SK(−) phagemid DNA (pSK) was labeled at the 5′ ends, and reactions were carried out with recombinant top2α. VP-16 (100 μmol/L for 30 min) was included as a positive control. For testing top2β-mediated activity, recombinant top2β was used in the reactions as above with increasing concentrations of Dp44mT or with VP-16. B, apoptotic analysis of isogenic Nalm-6 leukemia cells (top2α/β +/+ , top2α +/− , and top2β −/− ) by propidium iodide staining and flow cytometry. The population of cells with sub-G 1 DNA content was compared at Dp44mT (0.1 μmol/L) or VP-16 (10 μmol/L) at 48 h. Representative of at least four independent experiments. The percentage of cells in each phase of cell cycle is provided. C, cellular topoisomerase cleavage complexes by top1, top2α, and top2β were determined using the immunocomplex of enzyme formation bioassay at 6 or 24 h as indicated in top2α/β wild-type Nalm-6 leukemic cells. Camptothecin (at 1 μmol/L) or VP-16 (at 100 μmol/L) was used as a positive control. Similar data were obtained in at least four independent experiments. D, Nalm-6 cells were also pretreated with pan-caspase inhibitor z-VAD-fmk (100 μmol/L for 30 min) and assayed for formation of nonapoptotic top2α cleavage complexes. E, Dp44mT sensitivity in siRNA-mediated top2α or top2β knockdown HeLa cells. Western blots indicate protein levels 48 h after siRNA transfection. Asterisks, statistically significant difference between the response in top2α +/− compared with top2α +/+ or top2β −/− cells. Bars, SD from two independent experiments.

    Techniques Used: Activity Assay, Labeling, Incubation, Recombinant, Positive Control, Staining, Flow Cytometry, Western Blot, Transfection

    3) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    4) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    5) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    6) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    7) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    8) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    9) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    10) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    11) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    12) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    13) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    14) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    15) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    16) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    17) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    18) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    19) Product Images from "Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells"

    Article Title: Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

    Journal:

    doi: 10.2353/ajpath.2008.071079

    TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).
    Figure Legend Snippet: TuBECs and BECs respond differently to various cytotoxic agents. TuBECs and BECs were treated with VP-16 ( A ; 10, 50 μmol/L), paclitaxel (Tax) ( B ; 3, 10 ng/ml), thapsigargin (Thap) ( C ; 10, 30 nmol/L), or temozolomide (Tmz) ( D ; 100, 300 μmol/L).

    Techniques Used:

    Related Articles

    Staining:

    Article Title: The DRY Box and C-Terminal Domain of the Human Cytomegalovirus US27 Gene Product Play a Role in Promoting Cell Growth and Survival
    Article Snippet: .. Apoptosis Assays Cells were seeded into 6-well dishes and treated with 10 µM etoposide (Sigma-Aldrich) for 48 hours, then harvested and stained with Annexin V and propidium iodide using the TACS Annexin V-FITC Staining Kit (Trevigen, Gaithersburg, MD) before analysis by flow cytometry. .. In addition, cells were seeded into white 96 well plates at a density of 5×103 cells per well in the presence of 10 µM etoposide, and cell viability determined at indicated time points via the addition of CellTiter-Glo reagent as above.

    Flow Cytometry:

    Article Title: The DRY Box and C-Terminal Domain of the Human Cytomegalovirus US27 Gene Product Play a Role in Promoting Cell Growth and Survival
    Article Snippet: .. Apoptosis Assays Cells were seeded into 6-well dishes and treated with 10 µM etoposide (Sigma-Aldrich) for 48 hours, then harvested and stained with Annexin V and propidium iodide using the TACS Annexin V-FITC Staining Kit (Trevigen, Gaithersburg, MD) before analysis by flow cytometry. .. In addition, cells were seeded into white 96 well plates at a density of 5×103 cells per well in the presence of 10 µM etoposide, and cell viability determined at indicated time points via the addition of CellTiter-Glo reagent as above.

    Selection:

    Article Title: Low Dose Ionizing Radiation Strongly Stimulates Insertional Mutagenesis in a γH2AX Dependent Manner
    Article Snippet: .. For etoposide treatment, electroporated cells were seeded into 10 cm dishes containing a range of etoposide (Sigma E1383, stock solution 10 mM in DMSO) concentrations in 10 ml media; after seeding 5 µl and 50 µl aliquots were taken and plated in triplicate into 6-well plates containing 2 ml media with the same etoposide concentration; media was replaced next day and selection started in 10 cm dishes. ..

    Cytometry:

    Article Title: The DRY Box and C-Terminal Domain of the Human Cytomegalovirus US27 Gene Product Play a Role in Promoting Cell Growth and Survival
    Article Snippet: .. Apoptosis Assays Cells were seeded into 6-well dishes and treated with 10 µM etoposide (Sigma-Aldrich) for 48 hours, then harvested and stained with Annexin V and propidium iodide using the TACS Annexin V-FITC Staining Kit (Trevigen, Gaithersburg, MD) before analysis by flow cytometry. .. In addition, cells were seeded into white 96 well plates at a density of 5×103 cells per well in the presence of 10 µM etoposide, and cell viability determined at indicated time points via the addition of CellTiter-Glo reagent as above.

    Concentration Assay:

    Article Title: Low Dose Ionizing Radiation Strongly Stimulates Insertional Mutagenesis in a γH2AX Dependent Manner
    Article Snippet: .. For etoposide treatment, electroporated cells were seeded into 10 cm dishes containing a range of etoposide (Sigma E1383, stock solution 10 mM in DMSO) concentrations in 10 ml media; after seeding 5 µl and 50 µl aliquots were taken and plated in triplicate into 6-well plates containing 2 ml media with the same etoposide concentration; media was replaced next day and selection started in 10 cm dishes. ..

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    Millipore materials etoposide
    SB203580 (SB) or SP600125 (SP) inhibit the formation of capillary-like structures and SB203580 cotreatment reduces migration and invasion of <t>etoposide-treated</t> cells. ( a ) Formation of capillary-like structures. Representative micrographs of the complete network of tubes formed by untreated (Ctr), treated (with etoposide, LY2940042, SB203580 or SP600125 alone) and cotreated cells (etoposide plus inhibitors). The negative control is obtained by cell exposure to 10 μ M sulforaphane. Original magnification × 10. The graph reports the number of branches of the tube network formed by cells under the treatment conditions as described above. Quantitative data are the means±S.D. of three independent experiments. °° P
    Materials Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 483 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/materials etoposide/product/Millipore
    Average 99 stars, based on 483 article reviews
    Price from $9.99 to $1999.99
    materials etoposide - by Bioz Stars, 2020-09
    99/100 stars
      Buy from Supplier

    Image Search Results


    SB203580 (SB) or SP600125 (SP) inhibit the formation of capillary-like structures and SB203580 cotreatment reduces migration and invasion of etoposide-treated cells. ( a ) Formation of capillary-like structures. Representative micrographs of the complete network of tubes formed by untreated (Ctr), treated (with etoposide, LY2940042, SB203580 or SP600125 alone) and cotreated cells (etoposide plus inhibitors). The negative control is obtained by cell exposure to 10 μ M sulforaphane. Original magnification × 10. The graph reports the number of branches of the tube network formed by cells under the treatment conditions as described above. Quantitative data are the means±S.D. of three independent experiments. °° P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: SB203580 (SB) or SP600125 (SP) inhibit the formation of capillary-like structures and SB203580 cotreatment reduces migration and invasion of etoposide-treated cells. ( a ) Formation of capillary-like structures. Representative micrographs of the complete network of tubes formed by untreated (Ctr), treated (with etoposide, LY2940042, SB203580 or SP600125 alone) and cotreated cells (etoposide plus inhibitors). The negative control is obtained by cell exposure to 10 μ M sulforaphane. Original magnification × 10. The graph reports the number of branches of the tube network formed by cells under the treatment conditions as described above. Quantitative data are the means±S.D. of three independent experiments. °° P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: Migration, Negative Control

    SB203580 (SB) reduces COX-2, ICAM-1, CXCR4 levels and MMP9 activity in etoposide-treated cells. Immunoblot analyses of COX-2 ( a ), ICAM-1 ( b ) and CXCR4 ( c ). The histograms summarize quantitative data of means±S.D. of three independent experiments. °° P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: SB203580 (SB) reduces COX-2, ICAM-1, CXCR4 levels and MMP9 activity in etoposide-treated cells. Immunoblot analyses of COX-2 ( a ), ICAM-1 ( b ) and CXCR4 ( c ). The histograms summarize quantitative data of means±S.D. of three independent experiments. °° P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: Activity Assay

    Etoposide activates p38MAPK, Akt and JNK. ( a ) Protein levels of PKC δ and α in cells treated with etoposide (1.25–100 μ M). Immunoblots shown are representative of three independent experiments. β -Actin is the internal loading control. ( b ) p38MAPK, JNK and Akt activation. Histograms summarize quantitative data of means±S.D. of three independent experiments. * P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: Etoposide activates p38MAPK, Akt and JNK. ( a ) Protein levels of PKC δ and α in cells treated with etoposide (1.25–100 μ M). Immunoblots shown are representative of three independent experiments. β -Actin is the internal loading control. ( b ) p38MAPK, JNK and Akt activation. Histograms summarize quantitative data of means±S.D. of three independent experiments. * P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: Western Blot, Activation Assay

    SB203580 cotreatment markedly reduces migration, invasion and MMP9 activity of etoposide-treated cells. ( a ) Formation of capillary-like structures. Representative micrographs of the complete network of tubes in untreated (Ctr) and treated cells. Original magnification × 10. ( b ) Immunoblot analysis of VEGF. The histogram summarizes quantitative data of means±S.D. of three independent experiments °° P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: SB203580 cotreatment markedly reduces migration, invasion and MMP9 activity of etoposide-treated cells. ( a ) Formation of capillary-like structures. Representative micrographs of the complete network of tubes in untreated (Ctr) and treated cells. Original magnification × 10. ( b ) Immunoblot analysis of VEGF. The histogram summarizes quantitative data of means±S.D. of three independent experiments °° P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: Migration, Activity Assay

    Effects of SB203580 (SB) cotreatment on cell viability, clonogenicity and formation of NBSs. ( a ) Left panel, cell viability. Cells were pre-treated for 1 h with the different inhibitors (0.1 μ M chelerythrine chloride (Chele), 500 nM LY2940042 (LY), 50 μ M PD98059 (PD), 10 μ M SB203580 or 4 μ M SP600125 (SP)) and then exposed to 1.25 μ M etoposide for an additional 24 h. Histogram summarizes quantitative data of means±S.D. of five independent experiments. * P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: Effects of SB203580 (SB) cotreatment on cell viability, clonogenicity and formation of NBSs. ( a ) Left panel, cell viability. Cells were pre-treated for 1 h with the different inhibitors (0.1 μ M chelerythrine chloride (Chele), 500 nM LY2940042 (LY), 50 μ M PD98059 (PD), 10 μ M SB203580 or 4 μ M SP600125 (SP)) and then exposed to 1.25 μ M etoposide for an additional 24 h. Histogram summarizes quantitative data of means±S.D. of five independent experiments. * P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques:

    Etoposide decreases cell viability and, at high drug concentrations, inhibits the tumorigenic potential of HTLA-230 NB cells and prevents NBS formation. ( a ) Cell viability was determined by MTT assays in cells exposed to increasing concentrations of etoposide (0.07–225 μ M) for 24 h. Histograms summarize quantitative data of means±S.D. of five independent experiments. * P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: Etoposide decreases cell viability and, at high drug concentrations, inhibits the tumorigenic potential of HTLA-230 NB cells and prevents NBS formation. ( a ) Cell viability was determined by MTT assays in cells exposed to increasing concentrations of etoposide (0.07–225 μ M) for 24 h. Histograms summarize quantitative data of means±S.D. of five independent experiments. * P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: MTT Assay

    Effects of SB203580 (SB) cotreatment on viability, clonogenicity, CC133/Oct4 expression and p38MAPK activation in SK-N-SH and IMR-32 cells. ( a ) Cell viability. SK-N-SH (left panel) and IMR-32 (right panel) cells were exposed to increasing concentrations of etoposide (0.07–225 μ M) for 24 h. Histograms summarize quantitative data of means±S.D. of five independent experiments. * P

    Journal: Cell Death & Disease

    Article Title: p38MAPK inhibition: a new combined approach to reduce neuroblastoma resistance under etoposide treatment

    doi: 10.1038/cddis.2013.118

    Figure Lengend Snippet: Effects of SB203580 (SB) cotreatment on viability, clonogenicity, CC133/Oct4 expression and p38MAPK activation in SK-N-SH and IMR-32 cells. ( a ) Cell viability. SK-N-SH (left panel) and IMR-32 (right panel) cells were exposed to increasing concentrations of etoposide (0.07–225 μ M) for 24 h. Histograms summarize quantitative data of means±S.D. of five independent experiments. * P

    Article Snippet: Materials Etoposide, chelerythrine chloride, LY2940042 and PD98059 were obtained from Calbiochem (Merck KGaA, Darmstadt, Germany).

    Techniques: Expressing, Activation Assay

    ( A ) Western blot analysis of HO-1 protein expression after HO-1 siRNA addition to CoPP-treated macrophages. RAW 264.7 macrophages were transfected with two different HO-1 siRNA sequences (1 and 2) and nonspecific control siRNA before CoPP treatment. Lanes 1 and 2 represent HO-1 siRNA sequences 1 and 2, respectively. Note: HO-1 siRNA sequence 2 inhibited CoPP-induced HO-1 protein induction, whereas sequence 1 and nonspecific siRNA had no effect on HO-1 expression. ( B ) Western blot analysis of HO-1 and caspase-3 gene products in Ad-HO-1-transfected YPEN-1 cells. The expression of HO-1 and caspase-3 was probed with rabbit anti-mouse HO-1 ( a ) and caspase-3 ( b ) antibodies. Lane 1, YPEN-1 cells alone; lane 2, YPEN-1 cells plus etoposide (50 μ M ); lane 3, YPEN-1 cells transfected with Ad-HO-1 and HO-1 siRNA plus etoposide (50 μ M ); lane 4, YPEN-1 cells transfected with Ad-HO-1 and nonspecific siRNA plus etoposide (50 μ M ); lane 5, YPEN-1 cells transfected with Ad-HO-1; lane 6, YPEN-1 cells transfected with Ad-β-gal. Note the selectively inhibited expression of HO-1 in HO-1 siRNA-treated YPEN-1 cells (lane 3a), as compared with nonspecific siRNA and Ad-HO-1 (lanes 4a and 5a). In contrast, the expression of caspase-3 increased in cells treated with 50 μ M etoposide (lane 2b) or after HO-1 siRNA (lane 3b) or Ad-β-gal (lane 6b), as compared with nonspecific siRNA (lane 4b) or Ad-HO-1 (lane 5b). Anti-β-actin antibody was used to ensure equal protein amounts between the samples. Data shown are representative of three separate experiments.

    Journal: Human Gene Therapy

    Article Title: Small Interfering RNA Targeting Heme Oxygenase-1 (HO-1) Reinforces Liver Apoptosis Induced by Ischemia-Reperfusion Injury in Mice: HO-1 Is Necessary for Cytoprotection

    doi: 10.1089/hum.2009.049

    Figure Lengend Snippet: ( A ) Western blot analysis of HO-1 protein expression after HO-1 siRNA addition to CoPP-treated macrophages. RAW 264.7 macrophages were transfected with two different HO-1 siRNA sequences (1 and 2) and nonspecific control siRNA before CoPP treatment. Lanes 1 and 2 represent HO-1 siRNA sequences 1 and 2, respectively. Note: HO-1 siRNA sequence 2 inhibited CoPP-induced HO-1 protein induction, whereas sequence 1 and nonspecific siRNA had no effect on HO-1 expression. ( B ) Western blot analysis of HO-1 and caspase-3 gene products in Ad-HO-1-transfected YPEN-1 cells. The expression of HO-1 and caspase-3 was probed with rabbit anti-mouse HO-1 ( a ) and caspase-3 ( b ) antibodies. Lane 1, YPEN-1 cells alone; lane 2, YPEN-1 cells plus etoposide (50 μ M ); lane 3, YPEN-1 cells transfected with Ad-HO-1 and HO-1 siRNA plus etoposide (50 μ M ); lane 4, YPEN-1 cells transfected with Ad-HO-1 and nonspecific siRNA plus etoposide (50 μ M ); lane 5, YPEN-1 cells transfected with Ad-HO-1; lane 6, YPEN-1 cells transfected with Ad-β-gal. Note the selectively inhibited expression of HO-1 in HO-1 siRNA-treated YPEN-1 cells (lane 3a), as compared with nonspecific siRNA and Ad-HO-1 (lanes 4a and 5a). In contrast, the expression of caspase-3 increased in cells treated with 50 μ M etoposide (lane 2b) or after HO-1 siRNA (lane 3b) or Ad-β-gal (lane 6b), as compared with nonspecific siRNA (lane 4b) or Ad-HO-1 (lane 5b). Anti-β-actin antibody was used to ensure equal protein amounts between the samples. Data shown are representative of three separate experiments.

    Article Snippet: After washing, cells were treated with 50 μ M etoposide (Calbiochem, San Diego, CA) in YPEN-1 cultures for 2 hr or cells were treated with cobalt protoporphyrin (CoPP, an HO-1 inducer, 10 μg/ml; Porphyrin Products, Logan, UT).

    Techniques: Western Blot, Expressing, Transfection, Sequencing

    p38 and BiP inhibit Bax activation A , Western blot analysis of Bax levels in T-Hep3 and D-HEp3 cells treated with SB203580 for 48 hours. B , the indicated cells treated with or without doxorubicin ( Dox , 1 μg/mL) or etoposide ( Et ). The slight nuclear staining was due to doxorubicin emitting a low signal that crossed into the FITC channel ( b ). a, inset , plane of focus that sectioned the nucleus, to illustrate that the Bax signal is excluded from the nucleus. Bar, 40 μm. C , FACS analysis of T-Hep3 or D-HEp3 cells treated with 40 μmol/L etoposide for 24 hours and then stained with 6A7 mAb ( top ) or an isotype-matched IgG ( bottom ). The signal was developed using an Alexa-488–conjugated goat anti-mouse antibody and quantitated through FACS. D , Bax activation in control or BiP siRNA–transfected cells treated with or without 2 μg/mL doxorubicin was analyzed by immunofluorescence as in B ( D, top ). Nonspecific nuclear fluorescence due to doxorubicin accumulation in cells crossed to the FITC channel ( arrowheads ). Bar, 40 μm ( D, bottom ). E , Western blot analysis showing that total Bax levels are unaffected following siRNA mediated down-regulation of BiP. GAPDH was used as a loading control. F , quantitation of Bax activation in SB-treated or BiP siRNA–transfected cells treated with or without doxorubicin (2 μg/mL). Columns , mean of % Bax-positive cells in each sample; bars , SD. *, P

    Journal: Cancer research

    Article Title: Functional Coupling of p38-Induced Up-regulation of BiP and Activation of RNA-Dependent Protein Kinase–Like Endoplasmic Reticulum Kinase to Drug Resistance of Dormant Carcinoma Cells

    doi: 10.1158/0008-5472.CAN-05-3092

    Figure Lengend Snippet: p38 and BiP inhibit Bax activation A , Western blot analysis of Bax levels in T-Hep3 and D-HEp3 cells treated with SB203580 for 48 hours. B , the indicated cells treated with or without doxorubicin ( Dox , 1 μg/mL) or etoposide ( Et ). The slight nuclear staining was due to doxorubicin emitting a low signal that crossed into the FITC channel ( b ). a, inset , plane of focus that sectioned the nucleus, to illustrate that the Bax signal is excluded from the nucleus. Bar, 40 μm. C , FACS analysis of T-Hep3 or D-HEp3 cells treated with 40 μmol/L etoposide for 24 hours and then stained with 6A7 mAb ( top ) or an isotype-matched IgG ( bottom ). The signal was developed using an Alexa-488–conjugated goat anti-mouse antibody and quantitated through FACS. D , Bax activation in control or BiP siRNA–transfected cells treated with or without 2 μg/mL doxorubicin was analyzed by immunofluorescence as in B ( D, top ). Nonspecific nuclear fluorescence due to doxorubicin accumulation in cells crossed to the FITC channel ( arrowheads ). Bar, 40 μm ( D, bottom ). E , Western blot analysis showing that total Bax levels are unaffected following siRNA mediated down-regulation of BiP. GAPDH was used as a loading control. F , quantitation of Bax activation in SB-treated or BiP siRNA–transfected cells treated with or without doxorubicin (2 μg/mL). Columns , mean of % Bax-positive cells in each sample; bars , SD. *, P

    Article Snippet: SB203580 and etoposide were from Calbiochem (Beverly, MA).

    Techniques: Activation Assay, Western Blot, Staining, FACS, Transfection, Immunofluorescence, Fluorescence, Quantitation Assay

    T-HEp3 and D-HEp3 cell resistance to chemotherapy-induced apoptosis A , photomicrographs showing T-Hep3 and D-HEp3 cells treated with or without doxorubicin ( Dox ) for 30 hours in serum containing media. Bar, 160 μm. B , T-HEp3 and D-HEp3 cells treated with or without the indicated concentrations of doxorubicin or etoposide for 30 hours in serum containing media were detached with trypsin/EDTA and counted using a Coulter counter. C , cell viability assays using trypan blue exclusion test for T-HEp3 (□), D-HEp3 (◇) treated with or without the indicated concentrations of doxorubicin or etoposide for 30 hours. D , quantitation of DNA breaks as measured using the TUNEL assay Apo-Direct kit. Cells were counterstained with propidium iodide ( PI ) to detect all DNA content, and a positive control provided by the kit is shown in the top left dot plot. Apoptotic cells with labeled DNA breaks accumulate in the top left quadrant (D1, positive control or B1 in samples). Points , mean of % FITC-dUTP–positive cells in each sample ( bottom left ); bars , SD. + C , positive control. E , T-HEp3 and D-HEp3 cells were treated with the indicated concentrations of tunicamycin or thapsigargin for 16 hours, and the percentage of viable cells was determined by trypan blue exclusion assay as in ( B ).

    Journal: Cancer research

    Article Title: Functional Coupling of p38-Induced Up-regulation of BiP and Activation of RNA-Dependent Protein Kinase–Like Endoplasmic Reticulum Kinase to Drug Resistance of Dormant Carcinoma Cells

    doi: 10.1158/0008-5472.CAN-05-3092

    Figure Lengend Snippet: T-HEp3 and D-HEp3 cell resistance to chemotherapy-induced apoptosis A , photomicrographs showing T-Hep3 and D-HEp3 cells treated with or without doxorubicin ( Dox ) for 30 hours in serum containing media. Bar, 160 μm. B , T-HEp3 and D-HEp3 cells treated with or without the indicated concentrations of doxorubicin or etoposide for 30 hours in serum containing media were detached with trypsin/EDTA and counted using a Coulter counter. C , cell viability assays using trypan blue exclusion test for T-HEp3 (□), D-HEp3 (◇) treated with or without the indicated concentrations of doxorubicin or etoposide for 30 hours. D , quantitation of DNA breaks as measured using the TUNEL assay Apo-Direct kit. Cells were counterstained with propidium iodide ( PI ) to detect all DNA content, and a positive control provided by the kit is shown in the top left dot plot. Apoptotic cells with labeled DNA breaks accumulate in the top left quadrant (D1, positive control or B1 in samples). Points , mean of % FITC-dUTP–positive cells in each sample ( bottom left ); bars , SD. + C , positive control. E , T-HEp3 and D-HEp3 cells were treated with the indicated concentrations of tunicamycin or thapsigargin for 16 hours, and the percentage of viable cells was determined by trypan blue exclusion assay as in ( B ).

    Article Snippet: SB203580 and etoposide were from Calbiochem (Beverly, MA).

    Techniques: Quantitation Assay, TUNEL Assay, Positive Control, Labeling, Trypan Blue Exclusion Assay

    (A) Cell death percentage of Caki-1, mock and RNA interference clone no.2 cells detected by MTT. (B) Time course measurement of the apoptotic cell percentage of Caki-1 and XIAP no-expression Caki-1 cells following Etoposide treatment. As assessed by flow cytometry. Data are expressed as the mean ± standard deviation. *P

    Journal: Molecular Medicine Reports

    Article Title: XIAP underlies apoptosis resistance of renal cell carcinoma cells

    doi: 10.3892/mmr.2017.7925

    Figure Lengend Snippet: (A) Cell death percentage of Caki-1, mock and RNA interference clone no.2 cells detected by MTT. (B) Time course measurement of the apoptotic cell percentage of Caki-1 and XIAP no-expression Caki-1 cells following Etoposide treatment. As assessed by flow cytometry. Data are expressed as the mean ± standard deviation. *P

    Article Snippet: Measurement of cell viability and cell apoptosis CH11 (cat. no. 49516; 37°C for 24 h) from Abcam (Cambridge, MA, USA), Topotecan (cat. no. d1916; 37°C for 24 h) from Baomanbio (Shanghai, China), CAPE (cat. no. 211200; 37°C for 24 h) from Calbiochem; Merck KGaA (Darmstadt, Germany), and Etoposide (cat. no. 341205; 37°C for 24 h) from Calbiochem were used to induce apoptosis, and cell viability was detected by counting cells under the optical microscope.

    Techniques: MTT Assay, Expressing, Flow Cytometry, Cytometry, Standard Deviation

    XIAP protein expression levels following Etoposide treatment, as assessed by western blot analysis. XIAP, X-linked inhibitor of apoptosis.

    Journal: Molecular Medicine Reports

    Article Title: XIAP underlies apoptosis resistance of renal cell carcinoma cells

    doi: 10.3892/mmr.2017.7925

    Figure Lengend Snippet: XIAP protein expression levels following Etoposide treatment, as assessed by western blot analysis. XIAP, X-linked inhibitor of apoptosis.

    Article Snippet: Measurement of cell viability and cell apoptosis CH11 (cat. no. 49516; 37°C for 24 h) from Abcam (Cambridge, MA, USA), Topotecan (cat. no. d1916; 37°C for 24 h) from Baomanbio (Shanghai, China), CAPE (cat. no. 211200; 37°C for 24 h) from Calbiochem; Merck KGaA (Darmstadt, Germany), and Etoposide (cat. no. 341205; 37°C for 24 h) from Calbiochem were used to induce apoptosis, and cell viability was detected by counting cells under the optical microscope.

    Techniques: Expressing, Western Blot

    Cell viability percentage of ClearCa-2 and ClearCa-6 cell lines following CH11, Topotecan, CAPE and Etoposide treatment. Data are expressed as the mean ± standard deviation. *P

    Journal: Molecular Medicine Reports

    Article Title: XIAP underlies apoptosis resistance of renal cell carcinoma cells

    doi: 10.3892/mmr.2017.7925

    Figure Lengend Snippet: Cell viability percentage of ClearCa-2 and ClearCa-6 cell lines following CH11, Topotecan, CAPE and Etoposide treatment. Data are expressed as the mean ± standard deviation. *P

    Article Snippet: Measurement of cell viability and cell apoptosis CH11 (cat. no. 49516; 37°C for 24 h) from Abcam (Cambridge, MA, USA), Topotecan (cat. no. d1916; 37°C for 24 h) from Baomanbio (Shanghai, China), CAPE (cat. no. 211200; 37°C for 24 h) from Calbiochem; Merck KGaA (Darmstadt, Germany), and Etoposide (cat. no. 341205; 37°C for 24 h) from Calbiochem were used to induce apoptosis, and cell viability was detected by counting cells under the optical microscope.

    Techniques: Standard Deviation