etoposide  (LKT Laboratories)

 
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    Name:
    Etoposide
    Description:
    Podophyllotoxin derivative topoisomerase II inhibitor
    Catalog Number:
    e7657
    Price:
    81.9
    Purity:
    ≥98%
    Size:
    100 mg
    Category:
    Cancer Biology
    Buy from Supplier


    Structured Review

    LKT Laboratories etoposide
    Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to <t>etoposide</t> or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .
    Podophyllotoxin derivative topoisomerase II inhibitor
    https://www.bioz.com/result/etoposide/product/LKT Laboratories
    Average 86 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    etoposide - by Bioz Stars, 2020-09
    86/100 stars

    Images

    1) Product Images from "Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks"

    Article Title: Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks

    Journal: Environmental and molecular mutagenesis

    doi: 10.1002/em.22245

    Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to etoposide or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .
    Figure Legend Snippet: Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to etoposide or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .

    Techniques Used: Non-Homologous End Joining, Translocation Assay, Microscopy, Negative Control, Fluorescence

    γH2AX foci as marker of DNA damage observed 1 hr post-exposure to tested compounds at approximate calculated LD50 dose. (A) DMSO vehicle only. (B) etoposide 12.5μM. (C-F) flavonols— (C) quercetin 75μM, (D) kaempferol 100μM, (E) myricetin 50μM, (F) fisetin 25μM. (G-I) isoflavones— (G) genistein 75μM, (H) daidzein 200μM, (I) biochaninA 200μM. (J-K) flavones— (J) luteolin 200μM, (K) flavone 200μM. (L) flavanone narigenin 200μM.
    Figure Legend Snippet: γH2AX foci as marker of DNA damage observed 1 hr post-exposure to tested compounds at approximate calculated LD50 dose. (A) DMSO vehicle only. (B) etoposide 12.5μM. (C-F) flavonols— (C) quercetin 75μM, (D) kaempferol 100μM, (E) myricetin 50μM, (F) fisetin 25μM. (G-I) isoflavones— (G) genistein 75μM, (H) daidzein 200μM, (I) biochaninA 200μM. (J-K) flavones— (J) luteolin 200μM, (K) flavone 200μM. (L) flavanone narigenin 200μM.

    Techniques Used: Marker

    Related Articles

    Injection:

    Article Title: Spinocerebellar ataxia with axonal neuropathy: consequence of a Tdp1 recessive neomorphic mutation?
    Article Snippet: .. Bleomycin (Bristol-Myers Squibb, Montreal, Canada), CPT-11 (Yakult Honsha Co., Tokyo, Japan), etoposide (Novapharm, Toronto, Canada), or topotecan (LKT laboratories, Inc.) were diluted with 5% Dextrose solution prior to intraperitoneal injection. .. Drug or PBS was given to five wild-type and five Tdp1 −/− mice according to the dosages and administration schedules indicated in the Results and .

    other:

    Article Title: Smac mimetics increase cancer cell response to chemotherapeutics in a TNF-?-dependent manner
    Article Snippet: Etoposide and 5-FU were obtained from LKT Laboratory (St Paul, MN, USA).

    Article Title: Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks
    Article Snippet: Etoposide, all flavonoids, and vitamins were obtained from LKT Laboratories.

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage
    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Cycling Probe Technology:

    Article Title: Spinocerebellar ataxia with axonal neuropathy: consequence of a Tdp1 recessive neomorphic mutation?
    Article Snippet: .. Bleomycin (Bristol-Myers Squibb, Montreal, Canada), CPT-11 (Yakult Honsha Co., Tokyo, Japan), etoposide (Novapharm, Toronto, Canada), or topotecan (LKT laboratories, Inc.) were diluted with 5% Dextrose solution prior to intraperitoneal injection. .. Drug or PBS was given to five wild-type and five Tdp1 −/− mice according to the dosages and administration schedules indicated in the Results and .

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  • 93
    LKT Laboratories etoposide
    Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to <t>etoposide</t> or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .
    Etoposide, supplied by LKT Laboratories, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/etoposide/product/LKT Laboratories
    Average 93 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    etoposide - by Bioz Stars, 2020-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to etoposide or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .

    Journal: Environmental and molecular mutagenesis

    Article Title: Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks

    doi: 10.1002/em.22245

    Figure Lengend Snippet: Cellular characterization of GFP+ HSC colonies resulting from illegitimate NHEJ DNA repair and a chromosomal translocation following exposure to etoposide or bioflavonoids. (A-H) GFP+ HSC colonies were scored by inverted fluorescent microscopy beginning 96 hrs post-exposure. Representative phase contrast (left panels) and fluorescent (right panels) microscopy images of GFP+ colonies are shown side by side. (A,B) negative control. (C,D) + etoposide. (E,F) + genistein. (G,H) + quercetin. The lack of background fluorescence in the assay is demonstrated in negative control (A) and one of the two colonies in the field following etoposide exposure (D) .

    Article Snippet: Etoposide, all flavonoids, and vitamins were obtained from LKT Laboratories.

    Techniques: Non-Homologous End Joining, Translocation Assay, Microscopy, Negative Control, Fluorescence

    γH2AX foci as marker of DNA damage observed 1 hr post-exposure to tested compounds at approximate calculated LD50 dose. (A) DMSO vehicle only. (B) etoposide 12.5μM. (C-F) flavonols— (C) quercetin 75μM, (D) kaempferol 100μM, (E) myricetin 50μM, (F) fisetin 25μM. (G-I) isoflavones— (G) genistein 75μM, (H) daidzein 200μM, (I) biochaninA 200μM. (J-K) flavones— (J) luteolin 200μM, (K) flavone 200μM. (L) flavanone narigenin 200μM.

    Journal: Environmental and molecular mutagenesis

    Article Title: Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks

    doi: 10.1002/em.22245

    Figure Lengend Snippet: γH2AX foci as marker of DNA damage observed 1 hr post-exposure to tested compounds at approximate calculated LD50 dose. (A) DMSO vehicle only. (B) etoposide 12.5μM. (C-F) flavonols— (C) quercetin 75μM, (D) kaempferol 100μM, (E) myricetin 50μM, (F) fisetin 25μM. (G-I) isoflavones— (G) genistein 75μM, (H) daidzein 200μM, (I) biochaninA 200μM. (J-K) flavones— (J) luteolin 200μM, (K) flavone 200μM. (L) flavanone narigenin 200μM.

    Article Snippet: Etoposide, all flavonoids, and vitamins were obtained from LKT Laboratories.

    Techniques: Marker

    Induction of (A) p-H2AX, (B) total p53, (C) p-p53(ser15), and (D–F) p53 effector proteins following 24-h etoposide, quercetin, and methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). The lowest statistically significant ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Induction of (A) p-H2AX, (B) total p53, (C) p-p53(ser15), and (D–F) p53 effector proteins following 24-h etoposide, quercetin, and methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). The lowest statistically significant ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques:

    Time- and concentration-dependent response for p-p53(ser15) induction in HT1080 cells following exposure to (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate. Cells were treated with DMSO (0.1%), etoposide, quercetin, or methyl methanesulfonate for 1, 2, 4, 6, 8, 16, or 24 h and analyzed for p-p53 using flow cytometry. Circles and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Bars represent the standard error of the mean (SEM).

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Time- and concentration-dependent response for p-p53(ser15) induction in HT1080 cells following exposure to (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate. Cells were treated with DMSO (0.1%), etoposide, quercetin, or methyl methanesulfonate for 1, 2, 4, 6, 8, 16, or 24 h and analyzed for p-p53 using flow cytometry. Circles and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Bars represent the standard error of the mean (SEM).

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Concentration Assay, Flow Cytometry, Cytometry

    Characterization of the damage mechanism-independent p53 response. (A) Venn diagram of genes differentially expressed genes regulated by p53 following exposure to etoposide, quercetin, or methyl methanesulfonate, which have been previously shown to be regulated by p53 binding. (B) Functional annotation graph of Gene Ontology (GO) terms enriched in the genes regulated by p53 and differentially expressed in response to exposure to all three chemicals. Terms are connected according to the structure of the parent-child relationships defined by GO. Blue terms are statistically enriched, relative to their prevalence in the genome ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Characterization of the damage mechanism-independent p53 response. (A) Venn diagram of genes differentially expressed genes regulated by p53 following exposure to etoposide, quercetin, or methyl methanesulfonate, which have been previously shown to be regulated by p53 binding. (B) Functional annotation graph of Gene Ontology (GO) terms enriched in the genes regulated by p53 and differentially expressed in response to exposure to all three chemicals. Terms are connected according to the structure of the parent-child relationships defined by GO. Blue terms are statistically enriched, relative to their prevalence in the genome ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Binding Assay, Functional Assay

    Induction of (A) p-p53(ser46), (B) apoptosis, and (C) necrosis following 24-h etoposide, quercetin, and methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). (B) Apoptosis indicates the percent of cells stained positive for cleaved caspase 3. (C) Necrosis indicates the percent of cells stained positive for membrane permeability dye. (D) Late apoptosis indicates percent of cells co-stained with cleaved caspase 3 and membrane permeability dye. The lowest statistically significant ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Induction of (A) p-p53(ser46), (B) apoptosis, and (C) necrosis following 24-h etoposide, quercetin, and methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). (B) Apoptosis indicates the percent of cells stained positive for cleaved caspase 3. (C) Necrosis indicates the percent of cells stained positive for membrane permeability dye. (D) Late apoptosis indicates percent of cells co-stained with cleaved caspase 3 and membrane permeability dye. The lowest statistically significant ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Staining, Permeability

    Induction of micronuclei following (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate treatment. Circles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). Insets show data for concentrations near the transition point on a linear scale, together with the model predicted using the Lutz and Lutz hockey stick model (Lutz and Lutz, 2009 ). The Lutz model p -values for the micronucleus curves were 0.30, 0.99, and 0.048 for etoposide, quercetin, and methyl methanesulfonate, respectively. The lowest statistically significant ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Induction of micronuclei following (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate treatment. Circles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). Insets show data for concentrations near the transition point on a linear scale, together with the model predicted using the Lutz and Lutz hockey stick model (Lutz and Lutz, 2009 ). The Lutz model p -values for the micronucleus curves were 0.30, 0.99, and 0.048 for etoposide, quercetin, and methyl methanesulfonate, respectively. The lowest statistically significant ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques:

    Activation of protein and cell fate response at concentrations of etoposide, quercetin, or methyl methanesulfonate concentrations causing similar induction of p53. A p53-normalized concentration was established based on a similar level of p53 activation (approximately 25% of cells responding for total p53 at 24 h). This level of induction in p53 expression represents approximately half of the maximal induction observed with any of the three prototype chemicals. The resulting concentrations for comparison were 0.3-μM etoposide, 30-μM quercetin, and 200-μM methyl methanesulfonate. The degree of orange coloring indicates the degree of upregulation for a particular protein or process. For each endpoint, the percent of maximal response was calculated for each chemical. The response data were then divided into quintiles: 0–20%, 21–40%, 41–60%, 61–80%, and 81–100% of maximal response.

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Activation of protein and cell fate response at concentrations of etoposide, quercetin, or methyl methanesulfonate concentrations causing similar induction of p53. A p53-normalized concentration was established based on a similar level of p53 activation (approximately 25% of cells responding for total p53 at 24 h). This level of induction in p53 expression represents approximately half of the maximal induction observed with any of the three prototype chemicals. The resulting concentrations for comparison were 0.3-μM etoposide, 30-μM quercetin, and 200-μM methyl methanesulfonate. The degree of orange coloring indicates the degree of upregulation for a particular protein or process. For each endpoint, the percent of maximal response was calculated for each chemical. The response data were then divided into quintiles: 0–20%, 21–40%, 41–60%, 61–80%, and 81–100% of maximal response.

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Activation Assay, Concentration Assay, Expressing

    Cell viability in HT1080 cells after treatment with (A) etoposide, (B) quercetin, or (C) methyl methanesulfonate. Cells were treated with DMSO, etoposide, quercetin, or methyl methanesulfonate for 4, 24, or 48 h. Cell viability was measured using an intracellular ATP content luminescence assay. The y-axes indicate the relative luminescence of the treated samples compared with control samples. Circles (4 h), squares (24 h), and triangles (48 h) represent the mean of three independent experiments (three biological and three technical replicates). Cross bars represent the standard error of the mean (SEM) of the data. RLU: relative fluorescence units. Etoposide caused a statistically significant ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Cell viability in HT1080 cells after treatment with (A) etoposide, (B) quercetin, or (C) methyl methanesulfonate. Cells were treated with DMSO, etoposide, quercetin, or methyl methanesulfonate for 4, 24, or 48 h. Cell viability was measured using an intracellular ATP content luminescence assay. The y-axes indicate the relative luminescence of the treated samples compared with control samples. Circles (4 h), squares (24 h), and triangles (48 h) represent the mean of three independent experiments (three biological and three technical replicates). Cross bars represent the standard error of the mean (SEM) of the data. RLU: relative fluorescence units. Etoposide caused a statistically significant ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Luminescence Assay, Fluorescence

    Time course for DNA damage and p53 network response in HT1080 cells following exposure to etoposide, quercetin, or methyl methanesulfonate. Representative Western blots from three separate experiments are shown. HT1080 cells were exposed to 0.1% DMSO (control cells; Ctrl), 1-μM etoposide (ETP), 30-μM quercetin (QUE), or 200-μM methyl methanesulfonate (MMS) for 3, 8, or 24 h. Total cellular protein was isolated and subjected to immunoblot analysis. GAPDH was used as an internal control.

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Time course for DNA damage and p53 network response in HT1080 cells following exposure to etoposide, quercetin, or methyl methanesulfonate. Representative Western blots from three separate experiments are shown. HT1080 cells were exposed to 0.1% DMSO (control cells; Ctrl), 1-μM etoposide (ETP), 30-μM quercetin (QUE), or 200-μM methyl methanesulfonate (MMS) for 3, 8, or 24 h. Total cellular protein was isolated and subjected to immunoblot analysis. GAPDH was used as an internal control.

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: Western Blot, Isolation

    Cell cycle effects following 24-h (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). The lowest statistically significant ( p

    Journal: Toxicological Sciences

    Article Title: Profiling Dose-Dependent Activation of p53-Mediated Signaling Pathways by Chemicals with Distinct Mechanisms of DNA Damage

    doi: 10.1093/toxsci/kfu153

    Figure Lengend Snippet: Cell cycle effects following 24-h (A) etoposide, (B) quercetin, and (C) methyl methanesulfonate treatment. Circles, squares, and triangles represent the mean of three independent experiments (three biological replicates, each with three technical replicates). Cross bars represent the standard error of the mean (SEM). The lowest statistically significant ( p

    Article Snippet: Reagents and antibodies Etoposide (≥98%) (CAS no. 33419-42-0; Cat no. 152003; Lot no. 2249K) and quercetin (97%) (quercetin dehydrate; CAS no. 6151-25-3; Cat no. E7657; Lot no. 23925401) were purchased from LKT Laboratories and MP Biomedicals, respectively.

    Techniques: