etoposide eto Millipore Search Results


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  • 99
    Millipore etoposide
    Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 6147 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    97
    Millipore vp 16 etoposide
    Zap70 and Syk loss is a consequence of DNA damage, but not of caspase activation (A) Representative flow cytometry plots showing the proportions of isolated NK cells positive for anti-cleaved Caspase 3 antibody (top) or NK cells that are Zap70 low (bottom). NK cells from a single donor, either treated with DMSO (left column, control) or with 0.25mg/mL <t>VP-16</t> (right column) in DMSO, for 24 hours. Data are representative of 17 donors. (B) Percent of either Syk low , Zap70 low or cleaved Caspase 3 + in isolated NK cells from 9 donors following 24 hour treatment with 0.25mg/mL VP-16 <t>etoposide,</t> or DMSO control. (C) Percent of cleaved Caspase 3 + NK cells from 6 donors following 24 hour treatment with: DMSO control, 15uM Z-VAD-FMK caspase inhibitor alone, 0.25mg/mL VP-16 etoposide, or Z-VAD-FMK inhibitor and VP16 together. All cultures contained 500U/ml IL-2. Shown is the result of Tukey’s post test of paired ANOVA. (D) Percent of Zap70 low NK cells following 24 hour treatment, as in C, for seven donors. All panels show data that are representative of at least 3 independent experiments using NK cells from different donors. Statistical comparisons shown in all panels are the result of Tukey post-tests from paired 1-way or 2-way ANOVA, as appropriate. SEM are shown in all panels. **** = p
    Vp 16 Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 297 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Millipore etoposide eto
    Zap70 and Syk loss is a consequence of DNA damage, but not of caspase activation (A) Representative flow cytometry plots showing the proportions of isolated NK cells positive for anti-cleaved Caspase 3 antibody (top) or NK cells that are Zap70 low (bottom). NK cells from a single donor, either treated with DMSO (left column, control) or with 0.25mg/mL <t>VP-16</t> (right column) in DMSO, for 24 hours. Data are representative of 17 donors. (B) Percent of either Syk low , Zap70 low or cleaved Caspase 3 + in isolated NK cells from 9 donors following 24 hour treatment with 0.25mg/mL VP-16 <t>etoposide,</t> or DMSO control. (C) Percent of cleaved Caspase 3 + NK cells from 6 donors following 24 hour treatment with: DMSO control, 15uM Z-VAD-FMK caspase inhibitor alone, 0.25mg/mL VP-16 etoposide, or Z-VAD-FMK inhibitor and VP16 together. All cultures contained 500U/ml IL-2. Shown is the result of Tukey’s post test of paired ANOVA. (D) Percent of Zap70 low NK cells following 24 hour treatment, as in C, for seven donors. All panels show data that are representative of at least 3 independent experiments using NK cells from different donors. Statistical comparisons shown in all panels are the result of Tukey post-tests from paired 1-way or 2-way ANOVA, as appropriate. SEM are shown in all panels. **** = p
    Etoposide Eto, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Millipore etoposide etp
    Zap70 and Syk loss is a consequence of DNA damage, but not of caspase activation (A) Representative flow cytometry plots showing the proportions of isolated NK cells positive for anti-cleaved Caspase 3 antibody (top) or NK cells that are Zap70 low (bottom). NK cells from a single donor, either treated with DMSO (left column, control) or with 0.25mg/mL <t>VP-16</t> (right column) in DMSO, for 24 hours. Data are representative of 17 donors. (B) Percent of either Syk low , Zap70 low or cleaved Caspase 3 + in isolated NK cells from 9 donors following 24 hour treatment with 0.25mg/mL VP-16 <t>etoposide,</t> or DMSO control. (C) Percent of cleaved Caspase 3 + NK cells from 6 donors following 24 hour treatment with: DMSO control, 15uM Z-VAD-FMK caspase inhibitor alone, 0.25mg/mL VP-16 etoposide, or Z-VAD-FMK inhibitor and VP16 together. All cultures contained 500U/ml IL-2. Shown is the result of Tukey’s post test of paired ANOVA. (D) Percent of Zap70 low NK cells following 24 hour treatment, as in C, for seven donors. All panels show data that are representative of at least 3 independent experiments using NK cells from different donors. Statistical comparisons shown in all panels are the result of Tukey post-tests from paired 1-way or 2-way ANOVA, as appropriate. SEM are shown in all panels. **** = p
    Etoposide Etp, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Millipore m etoposide
    Flow cytometry (FACS analysis) of Jurkat cells treated with ( a ) 0.5 μ M staurosporine or ( b ) 50 μ M <t>etoposide.</t> In ( c ), treatments for 24 h were (1) 10 μ M rapamycin; (2) 50 μ M etoposide; (3) 50 μ M etoposide plus pan caspase inhibitor z-VAD-fmk; (4) 15 ng/ml TRAIL; (5) 15 ng/ml TRAIL plus z-VAD-fmk; (6) untreated. ( a – c ) ■, Annexin V-positive; ■, Annexin V-positive and mAb2C4:AF568-positive; ■, mAb2C4:AF568-positive and ■; double-negative, viable cells.
    M Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    78
    Millipore 100um etoposide
    Flow cytometry (FACS analysis) of Jurkat cells treated with ( a ) 0.5 μ M staurosporine or ( b ) 50 μ M <t>etoposide.</t> In ( c ), treatments for 24 h were (1) 10 μ M rapamycin; (2) 50 μ M etoposide; (3) 50 μ M etoposide plus pan caspase inhibitor z-VAD-fmk; (4) 15 ng/ml TRAIL; (5) 15 ng/ml TRAIL plus z-VAD-fmk; (6) untreated. ( a – c ) ■, Annexin V-positive; ■, Annexin V-positive and mAb2C4:AF568-positive; ■, mAb2C4:AF568-positive and ■; double-negative, viable cells.
    100um Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Millipore etoposide et
    Flow cytometry (FACS analysis) of Jurkat cells treated with ( a ) 0.5 μ M staurosporine or ( b ) 50 μ M <t>etoposide.</t> In ( c ), treatments for 24 h were (1) 10 μ M rapamycin; (2) 50 μ M etoposide; (3) 50 μ M etoposide plus pan caspase inhibitor z-VAD-fmk; (4) 15 ng/ml TRAIL; (5) 15 ng/ml TRAIL plus z-VAD-fmk; (6) untreated. ( a – c ) ■, Annexin V-positive; ■, Annexin V-positive and mAb2C4:AF568-positive; ■, mAb2C4:AF568-positive and ■; double-negative, viable cells.
    Etoposide Et, supplied by Millipore, used in various techniques. Bioz Stars score: 88/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore etoposide vp16
    Inhibition of RAD51 expression and <t>Etoposide</t> induces apoptosis in sphere cultures. (a) HeLa SPhere culture was exposed to 30 nM of siRAD51 and 5.8 μ g/mL of <t>VP16.</t> By MTT assay, cell viability was affected in the presence of both compounds, but not when they were added independently. The absence of RAD51 protein decreased the cell viability of spheres exposed to VP16. HeLa SP culture exposed to VP16 and 30 nM of random siRNA (scrambled) was used as control. (b and c) Apoptosis was evaluated by Annexin-V assay (see Materials and Methods) under identical conditions; the highest level of apoptosis was exhibited in the presence of both VP16 and siRAD51. The absence of RAD51 protein sensitized spheres to VP16. (d and e) Control indicating that treatment with siRAD51 and Etoposide induces apoptosis in ML cells. ∗∗ p
    Etoposide Vp16, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    82
    Millipore etoposide control
    Inhibition of RAD51 expression and <t>Etoposide</t> induces apoptosis in sphere cultures. (a) HeLa SPhere culture was exposed to 30 nM of siRAD51 and 5.8 μ g/mL of <t>VP16.</t> By MTT assay, cell viability was affected in the presence of both compounds, but not when they were added independently. The absence of RAD51 protein decreased the cell viability of spheres exposed to VP16. HeLa SP culture exposed to VP16 and 30 nM of random siRNA (scrambled) was used as control. (b and c) Apoptosis was evaluated by Annexin-V assay (see Materials and Methods) under identical conditions; the highest level of apoptosis was exhibited in the presence of both VP16 and siRAD51. The absence of RAD51 protein sensitized spheres to VP16. (d and e) Control indicating that treatment with siRAD51 and Etoposide induces apoptosis in ML cells. ∗∗ p
    Etoposide Control, supplied by Millipore, used in various techniques. Bioz Stars score: 82/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    80
    Millipore 10um etoposide
    Inhibition of RAD51 expression and <t>Etoposide</t> induces apoptosis in sphere cultures. (a) HeLa SPhere culture was exposed to 30 nM of siRAD51 and 5.8 μ g/mL of <t>VP16.</t> By MTT assay, cell viability was affected in the presence of both compounds, but not when they were added independently. The absence of RAD51 protein decreased the cell viability of spheres exposed to VP16. HeLa SP culture exposed to VP16 and 30 nM of random siRNA (scrambled) was used as control. (b and c) Apoptosis was evaluated by Annexin-V assay (see Materials and Methods) under identical conditions; the highest level of apoptosis was exhibited in the presence of both VP16 and siRAD51. The absence of RAD51 protein sensitized spheres to VP16. (d and e) Control indicating that treatment with siRAD51 and Etoposide induces apoptosis in ML cells. ∗∗ p
    10um Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 80/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    79
    Millipore rabbit anti vp 16
    GDNF and <t>VP-16</t> expression patterns . The GDNF expression pattern of the final ON group ( a , b ) was similar to that previously observed where the GDNF transgene (red) is observed distally from that of the transduced cells and VP-16 (green). ( b ) Increased magnification of area outlined in a . VP-16 expression in the OFF group ( c , d ) was similar to that seen in the ON group; however, no GDNF protein expression was observed. GDNF protein expression in the CBA-GDNF group ( e , f ) extended in a diffuse pattern into the VTA and the DMN indicating that GDNF protein was distributed away from the transduced cells in contrast to the pattern of expression observed from an intracellular transgene such as the SN-GFP group ( g , h ). As expected, no immunoreactivity was observed for VP-16 in either the CBA-GDNF group ( e , f , green) or the SN-GFP group ( g , h , red). ( f and h ) Higher magnifications of areas outlined in e and g , respectively. Bar: a , c , e , g = 1.0 mm, bar: b , d , f , h = 0.1 mm. CBA, chicken β-actin; DMN, deep mesencephalic nucleus; GDNF, glial cell line-derived neurotrophic factor; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulate; VTA, ventral tegmental area.
    Rabbit Anti Vp 16, supplied by Millipore, used in various techniques. Bioz Stars score: 79/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Millipore etoposide atp agarose
    GDNF and <t>VP-16</t> expression patterns . The GDNF expression pattern of the final ON group ( a , b ) was similar to that previously observed where the GDNF transgene (red) is observed distally from that of the transduced cells and VP-16 (green). ( b ) Increased magnification of area outlined in a . VP-16 expression in the OFF group ( c , d ) was similar to that seen in the ON group; however, no GDNF protein expression was observed. GDNF protein expression in the CBA-GDNF group ( e , f ) extended in a diffuse pattern into the VTA and the DMN indicating that GDNF protein was distributed away from the transduced cells in contrast to the pattern of expression observed from an intracellular transgene such as the SN-GFP group ( g , h ). As expected, no immunoreactivity was observed for VP-16 in either the CBA-GDNF group ( e , f , green) or the SN-GFP group ( g , h , red). ( f and h ) Higher magnifications of areas outlined in e and g , respectively. Bar: a , c , e , g = 1.0 mm, bar: b , d , f , h = 0.1 mm. CBA, chicken β-actin; DMN, deep mesencephalic nucleus; GDNF, glial cell line-derived neurotrophic factor; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulate; VTA, ventral tegmental area.
    Etoposide Atp Agarose, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore bone marrow suppressant vp 16
    Effects of engraftment location, estrogen, and immune suppressant on tumorigenicity of breast cancer cells NOD/SCID mice were treated ± 17β-estradiol (E 2 ) and <t>etoposide</t> as indicated. Six days later, mice were surgically incised and injected with 500 cells from a breast cancer pleural effusion in 25% Matrigel. A: final tumor volume. Data represent mean ± SE. B: tumor incidence. C: latency of tumor formation following injection (* P
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    Millipore topoisomerase ii inhibitor etoposide
    Effects of engraftment location, estrogen, and immune suppressant on tumorigenicity of breast cancer cells NOD/SCID mice were treated ± 17β-estradiol (E 2 ) and <t>etoposide</t> as indicated. Six days later, mice were surgically incised and injected with 500 cells from a breast cancer pleural effusion in 25% Matrigel. A: final tumor volume. Data represent mean ± SE. B: tumor incidence. C: latency of tumor formation following injection (* P
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    Millipore drug resistance against etoposide
    Effects of engraftment location, estrogen, and immune suppressant on tumorigenicity of breast cancer cells NOD/SCID mice were treated ± 17β-estradiol (E 2 ) and <t>etoposide</t> as indicated. Six days later, mice were surgically incised and injected with 500 cells from a breast cancer pleural effusion in 25% Matrigel. A: final tumor volume. Data represent mean ± SE. B: tumor incidence. C: latency of tumor formation following injection (* P
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    81
    Millipore topo ii inhibitor etoposide
    MMS22L foci form during S phase of the cell cycle and colocalize with HR proteins Immunofluorescence images of MMS22L foci formation at <t>etoposide</t> (ETP)‐induced DSBs during S, M, and G1 phases of the cell cycle in HeLa cells. Scale bar: 5 μm. Quantification of a representative experiment from (A) shows number of MMS22L foci per nucleus during indicated cell cycle phases ( n = 2; n nuclei ≥ 60). Immunofluorescence images of CPT‐induced MMS22L, RPA2, BRCA2, and RAD51 foci in U2OS cells. Scale bar: 5 μm. Quantification of a representative experiment ( n = 3) from (C) shows percentage of γH2AX, RPA2, BRCA2, and RAD51 foci colocalizing with MMS22L foci ( n nuclei = 30; nuclei with ≥ 25 MMS22L foci were analyzed). Data information: Boxplots in (B and D) represent distributions per nucleus; boxes indicate the 25–75 percentile and whiskers the 10–90 percentile. Horizontal lines mark the medians. Statistical analysis: Mann–Whitney U ‐test; *** P ≤ 0.0001; ns, not significant.
    Topo Ii Inhibitor Etoposide, supplied by Millipore, used in various techniques. Bioz Stars score: 81/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore etoposide 4 demethylepipodophyllotoxin 9 4 6 o ethylidene β d glucopyranoside
    MMS22L foci form during S phase of the cell cycle and colocalize with HR proteins Immunofluorescence images of MMS22L foci formation at <t>etoposide</t> (ETP)‐induced DSBs during S, M, and G1 phases of the cell cycle in HeLa cells. Scale bar: 5 μm. Quantification of a representative experiment from (A) shows number of MMS22L foci per nucleus during indicated cell cycle phases ( n = 2; n nuclei ≥ 60). Immunofluorescence images of CPT‐induced MMS22L, RPA2, BRCA2, and RAD51 foci in U2OS cells. Scale bar: 5 μm. Quantification of a representative experiment ( n = 3) from (C) shows percentage of γH2AX, RPA2, BRCA2, and RAD51 foci colocalizing with MMS22L foci ( n nuclei = 30; nuclei with ≥ 25 MMS22L foci were analyzed). Data information: Boxplots in (B and D) represent distributions per nucleus; boxes indicate the 25–75 percentile and whiskers the 10–90 percentile. Horizontal lines mark the medians. Statistical analysis: Mann–Whitney U ‐test; *** P ≤ 0.0001; ns, not significant.
    Etoposide 4 Demethylepipodophyllotoxin 9 4 6 O Ethylidene β D Glucopyranoside, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Precise quantification of individual treatment effects and monitoring of distinct clinical stages. a Imaging visualizes treatment-induced cell loss and regrowth; 10 5 ALL-50 cells/mouse were injected into 10 mice which received a single intraperitoneal dose of <t>Etoposid</t> (VP-16; 50 mg/kg) in week 6 after tumor cell injection, except the control mouse which was treated with PBS. Animals were imaged before treatment (pre-treatment) and 4 and 11 days after treatment; shown is one representative mouse; all mice are shown in Supplemental Figure 11; b, c Imaging visualizes different sensitivities of individual samples towards treatment; ALL-199 (1×10 4 cells/mouse) or ALL-4S (5×10 4 cells/mouse) were injected into 16 mice; mice were randomized in week 4 into one control (n = 4) and two experimental groups (n = 6 each). Control mice received buffer injection, while the other groups were treated once intraperitoneally with either Etoposid (VP-16; 50 mg/kg) or cyclophosphamide (Cyclo; 150 mg/kg) as indicated. Mice were imaged directly before and 4 days after treatment; shown are 3 representative mice of each treatment group before and 4 days after treatment ( b ); shown is the result of quantification of the images; each line represents a single mouse ( c ); * P
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    Precise quantification of individual treatment effects and monitoring of distinct clinical stages. a Imaging visualizes treatment-induced cell loss and regrowth; 10 5 ALL-50 cells/mouse were injected into 10 mice which received a single intraperitoneal dose of <t>Etoposid</t> (VP-16; 50 mg/kg) in week 6 after tumor cell injection, except the control mouse which was treated with PBS. Animals were imaged before treatment (pre-treatment) and 4 and 11 days after treatment; shown is one representative mouse; all mice are shown in Supplemental Figure 11; b, c Imaging visualizes different sensitivities of individual samples towards treatment; ALL-199 (1×10 4 cells/mouse) or ALL-4S (5×10 4 cells/mouse) were injected into 16 mice; mice were randomized in week 4 into one control (n = 4) and two experimental groups (n = 6 each). Control mice received buffer injection, while the other groups were treated once intraperitoneally with either Etoposid (VP-16; 50 mg/kg) or cyclophosphamide (Cyclo; 150 mg/kg) as indicated. Mice were imaged directly before and 4 days after treatment; shown are 3 representative mice of each treatment group before and 4 days after treatment ( b ); shown is the result of quantification of the images; each line represents a single mouse ( c ); * P
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    Precise quantification of individual treatment effects and monitoring of distinct clinical stages. a Imaging visualizes treatment-induced cell loss and regrowth; 10 5 ALL-50 cells/mouse were injected into 10 mice which received a single intraperitoneal dose of <t>Etoposid</t> (VP-16; 50 mg/kg) in week 6 after tumor cell injection, except the control mouse which was treated with PBS. Animals were imaged before treatment (pre-treatment) and 4 and 11 days after treatment; shown is one representative mouse; all mice are shown in Supplemental Figure 11; b, c Imaging visualizes different sensitivities of individual samples towards treatment; ALL-199 (1×10 4 cells/mouse) or ALL-4S (5×10 4 cells/mouse) were injected into 16 mice; mice were randomized in week 4 into one control (n = 4) and two experimental groups (n = 6 each). Control mice received buffer injection, while the other groups were treated once intraperitoneally with either Etoposid (VP-16; 50 mg/kg) or cyclophosphamide (Cyclo; 150 mg/kg) as indicated. Mice were imaged directly before and 4 days after treatment; shown are 3 representative mice of each treatment group before and 4 days after treatment ( b ); shown is the result of quantification of the images; each line represents a single mouse ( c ); * P
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    Image Search Results


    Zap70 and Syk loss is a consequence of DNA damage, but not of caspase activation (A) Representative flow cytometry plots showing the proportions of isolated NK cells positive for anti-cleaved Caspase 3 antibody (top) or NK cells that are Zap70 low (bottom). NK cells from a single donor, either treated with DMSO (left column, control) or with 0.25mg/mL VP-16 (right column) in DMSO, for 24 hours. Data are representative of 17 donors. (B) Percent of either Syk low , Zap70 low or cleaved Caspase 3 + in isolated NK cells from 9 donors following 24 hour treatment with 0.25mg/mL VP-16 etoposide, or DMSO control. (C) Percent of cleaved Caspase 3 + NK cells from 6 donors following 24 hour treatment with: DMSO control, 15uM Z-VAD-FMK caspase inhibitor alone, 0.25mg/mL VP-16 etoposide, or Z-VAD-FMK inhibitor and VP16 together. All cultures contained 500U/ml IL-2. Shown is the result of Tukey’s post test of paired ANOVA. (D) Percent of Zap70 low NK cells following 24 hour treatment, as in C, for seven donors. All panels show data that are representative of at least 3 independent experiments using NK cells from different donors. Statistical comparisons shown in all panels are the result of Tukey post-tests from paired 1-way or 2-way ANOVA, as appropriate. SEM are shown in all panels. **** = p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Human Natural Killer Cells Downregulate Zap70 and Syk in Response to Prolonged Activation or DNA Damage

    doi: 10.4049/jimmunol.1700542

    Figure Lengend Snippet: Zap70 and Syk loss is a consequence of DNA damage, but not of caspase activation (A) Representative flow cytometry plots showing the proportions of isolated NK cells positive for anti-cleaved Caspase 3 antibody (top) or NK cells that are Zap70 low (bottom). NK cells from a single donor, either treated with DMSO (left column, control) or with 0.25mg/mL VP-16 (right column) in DMSO, for 24 hours. Data are representative of 17 donors. (B) Percent of either Syk low , Zap70 low or cleaved Caspase 3 + in isolated NK cells from 9 donors following 24 hour treatment with 0.25mg/mL VP-16 etoposide, or DMSO control. (C) Percent of cleaved Caspase 3 + NK cells from 6 donors following 24 hour treatment with: DMSO control, 15uM Z-VAD-FMK caspase inhibitor alone, 0.25mg/mL VP-16 etoposide, or Z-VAD-FMK inhibitor and VP16 together. All cultures contained 500U/ml IL-2. Shown is the result of Tukey’s post test of paired ANOVA. (D) Percent of Zap70 low NK cells following 24 hour treatment, as in C, for seven donors. All panels show data that are representative of at least 3 independent experiments using NK cells from different donors. Statistical comparisons shown in all panels are the result of Tukey post-tests from paired 1-way or 2-way ANOVA, as appropriate. SEM are shown in all panels. **** = p

    Article Snippet: In experiments to study DNA damage and apoptosis in NK cells, VP-16 etoposide (Sigma Aldrich) and/or Z-VAD FMK (BD Biosciences) were included in the culture medium at concentrations of 0.25mg/ml and 15μM, respectively.

    Techniques: Activation Assay, Flow Cytometry, Cytometry, Isolation

    Band depletion and comet assay. A, Band depletion assay of the combination of RDC and etoposide produced more DNA-topo IIα complexes, depleting the topo IIα band in the Western blot analysis. These data indicate that blocking nuclear export

    Journal: Cancer research

    Article Title: Human Multiple Myeloma Cells Are Sensitized to Topoisomerase II Inhibitors by CRM1 Inhibition

    doi: 10.1158/0008-5472.CAN-09-0484

    Figure Lengend Snippet: Band depletion and comet assay. A, Band depletion assay of the combination of RDC and etoposide produced more DNA-topo IIα complexes, depleting the topo IIα band in the Western blot analysis. These data indicate that blocking nuclear export

    Article Snippet: Cells were treated with RDC for 16 hours followed by doxorubicin (2 μM; Sigma) for 4 hours or etoposide (VP-16; 10 μM; Sigma) for 7 hours and assayed for apoptosis by either anti-caspase 3 or TUNEL staining (BD Pharmingen).

    Techniques: Single Cell Gel Electrophoresis, Band Depletion Assay, Produced, Western Blot, Blocking Assay

    The normalized, relative expression of CDKN1A /p21 after DMSO or 8 hr of etoposide treatment (100 μM final) in a pilot RT-qPCR screen and in the experimental siRNA screen (A). Average (B) CDKN1A /p21, (C) BBC3 /puma, and (D) TP53 /p53 expression values under DMSO and etoposide conditions across each experimental RT-qPCR plate for nontargeting, TP53 , and MDM2 siRNA. Results from T-tests of pairwise comparisons can be found in Table 1 . DMSO, dimethyl sulfoxide; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; siRNA, small interfering RNA.

    Journal: G3: Genes|Genomes|Genetics

    Article Title: A Chromatin-Focused siRNA Screen for Regulators of p53-Dependent Transcription

    doi: 10.1534/g3.116.031534

    Figure Lengend Snippet: The normalized, relative expression of CDKN1A /p21 after DMSO or 8 hr of etoposide treatment (100 μM final) in a pilot RT-qPCR screen and in the experimental siRNA screen (A). Average (B) CDKN1A /p21, (C) BBC3 /puma, and (D) TP53 /p53 expression values under DMSO and etoposide conditions across each experimental RT-qPCR plate for nontargeting, TP53 , and MDM2 siRNA. Results from T-tests of pairwise comparisons can be found in Table 1 . DMSO, dimethyl sulfoxide; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; siRNA, small interfering RNA.

    Article Snippet: Each siRNA was delivered to 11,000 cells via reverse transfection using RNAiMax (Life Technologies) in a 96-well plate to a final concentration of 10 μM, media was changed after 24 hr, and cells were incubated for an additional 48 hr before addition of either DMSO or 100 μM (final) etoposide (Sigma-Aldrich) for 8 hr.

    Techniques: Expressing, Quantitative RT-PCR, Real-time Polymerase Chain Reaction, Small Interfering RNA

    TCP80 and RHA interact in vivo and cooperatively stimulate p53 expression in MCF-7 cells. (a) TCP80 has increased binding with RHA following DNA damage in MCF-7 cells. Subconfluent MCF-7 cells were treated with or without 10 μ M etoposide for 2 hours and then lysed with TGN buffer [ 8 ]. RHA was immunoprecipitated from the cell lysate as described in experimental procedures. The precipitated beads were then washed three times with TGN lysis buffer and SDS sample loading buffer was added. The samples were subjected to SDS-PAGE. An immunoblotting experiment was then performed to detect the TCP80 protein. The results presented are representative of three individual experiments. (b) Levels of TCP80 and RHA protein do not change following exposure to DNA damage in MCF-7 cells. MCF-7 cells were treated with 10 μ M etoposide for 2 hours and then lysed with TGN lysis buffer. The samples were subjected to SDS-PAGE. TCP80, RHA, and β -actin were detected by their respective antibodies. The results presented in (a) and (b) are representative of three individual experiments. (c) Overexpression of TCP80 and RHA leads to increased p53 expression in H1299 cells transfected with the pC53-SN3 vector. H1299 lung carcinoma cells (p53-null) were cotransfected with the p53 expression vector pC53-SN3 along with the empty pCDNA 3.1 vector, the TCP80 expression vector, or the TCP80 plus RHA expression vector. Twenty-four hours after transfection, the cells were treated with or without etoposide for 2 hours. Cells were then lysed, and equal amounts of protein were subjected to SDS-PAGE and transferred to a nitrocellulose membrane. The p53 protein and β -actin were then detected by their respective antibodies. (d) Statistical analysis of the expression levels of p53 (p53/ β -actin) between individual groups as shown in (c) was performed using one-way ANOVA with a Newman–Keul post hoc test from 4 sets of experimental results. Significance was assumed at ∗ P

    Journal: BioMed Research International

    Article Title: Translational Control Protein 80 Stimulates IRES-Mediated Translation of p53 mRNA in Response to DNA Damage

    doi: 10.1155/2015/708158

    Figure Lengend Snippet: TCP80 and RHA interact in vivo and cooperatively stimulate p53 expression in MCF-7 cells. (a) TCP80 has increased binding with RHA following DNA damage in MCF-7 cells. Subconfluent MCF-7 cells were treated with or without 10 μ M etoposide for 2 hours and then lysed with TGN buffer [ 8 ]. RHA was immunoprecipitated from the cell lysate as described in experimental procedures. The precipitated beads were then washed three times with TGN lysis buffer and SDS sample loading buffer was added. The samples were subjected to SDS-PAGE. An immunoblotting experiment was then performed to detect the TCP80 protein. The results presented are representative of three individual experiments. (b) Levels of TCP80 and RHA protein do not change following exposure to DNA damage in MCF-7 cells. MCF-7 cells were treated with 10 μ M etoposide for 2 hours and then lysed with TGN lysis buffer. The samples were subjected to SDS-PAGE. TCP80, RHA, and β -actin were detected by their respective antibodies. The results presented in (a) and (b) are representative of three individual experiments. (c) Overexpression of TCP80 and RHA leads to increased p53 expression in H1299 cells transfected with the pC53-SN3 vector. H1299 lung carcinoma cells (p53-null) were cotransfected with the p53 expression vector pC53-SN3 along with the empty pCDNA 3.1 vector, the TCP80 expression vector, or the TCP80 plus RHA expression vector. Twenty-four hours after transfection, the cells were treated with or without etoposide for 2 hours. Cells were then lysed, and equal amounts of protein were subjected to SDS-PAGE and transferred to a nitrocellulose membrane. The p53 protein and β -actin were then detected by their respective antibodies. (d) Statistical analysis of the expression levels of p53 (p53/ β -actin) between individual groups as shown in (c) was performed using one-way ANOVA with a Newman–Keul post hoc test from 4 sets of experimental results. Significance was assumed at ∗ P

    Article Snippet: Materials Etoposide was from Calbiochem.

    Techniques: In Vivo, Expressing, Binding Assay, Immunoprecipitation, Lysis, SDS Page, Over Expression, Transfection, Plasmid Preparation

    (a) MCF-7/shTCP80 cells express lower levels of TCP80 and RHA as compared to MCF-7 cells. MCF-7 and MCF-7/shTCP80 cells were grown to subconfluency. Cells were then lysed and equal amounts of protein were subjected to SDS-PAGE and western blotting. TCP80, RHA, and β -actin were detected by immunoblotting. (b) MCF-7/shTCP80 cells exhibit reduced induction of p53 and its downstream target PUMA following DNA damage. MCF-7 and MCF-7/shTCP80 cells were grown to subconfluency. Cells were then treated with 10 μ M etoposide for 2 hours. After the treatment, cells were lysed and equal amounts of protein were subjected to SDS-PAGE and transferred to PVDF membranes. p53, PUMA, and β -actin proteins were detected with their respective antibodies. (c) Statistical analysis of the expression levels of p53 (p53/ β -actin) between individual groups as seen in (b) was carried out using one-way ANOVA with a Newman–Keul post hoc test from 3 sets of experimental results. Significance was assumed at ∗ P

    Journal: BioMed Research International

    Article Title: Translational Control Protein 80 Stimulates IRES-Mediated Translation of p53 mRNA in Response to DNA Damage

    doi: 10.1155/2015/708158

    Figure Lengend Snippet: (a) MCF-7/shTCP80 cells express lower levels of TCP80 and RHA as compared to MCF-7 cells. MCF-7 and MCF-7/shTCP80 cells were grown to subconfluency. Cells were then lysed and equal amounts of protein were subjected to SDS-PAGE and western blotting. TCP80, RHA, and β -actin were detected by immunoblotting. (b) MCF-7/shTCP80 cells exhibit reduced induction of p53 and its downstream target PUMA following DNA damage. MCF-7 and MCF-7/shTCP80 cells were grown to subconfluency. Cells were then treated with 10 μ M etoposide for 2 hours. After the treatment, cells were lysed and equal amounts of protein were subjected to SDS-PAGE and transferred to PVDF membranes. p53, PUMA, and β -actin proteins were detected with their respective antibodies. (c) Statistical analysis of the expression levels of p53 (p53/ β -actin) between individual groups as seen in (b) was carried out using one-way ANOVA with a Newman–Keul post hoc test from 3 sets of experimental results. Significance was assumed at ∗ P

    Article Snippet: Materials Etoposide was from Calbiochem.

    Techniques: SDS Page, Western Blot, Expressing

    (a) TCP80 has increased binding to the p53 mRNA following DNA damage. MCF-7 cells were transfected with pcDNA3.1/HisB/TCP80 that encodes for the Xpress-tagged TCP80 protein. Twenty-four hours following transfection, the cells were treated with or without 10 μ M etoposide for 2 hours. They were then lysed in polysome lysis buffer and incubated with protein G-plus agarose beads coated with the anti-Xpress antibody. The TCP80 and mRNA complexes (mRNP) were immunoprecipitated and mRNA was extracted from the immunoprecipitate as described in Experimental procedures. RT-PCR was then performed to reverse-transcribe and amplify the p53 IRES sequence (~145 bp). (b) TCP80 positively affects the p53 IRES activity in response to DNA damage. MCF-7 cells were cotransfected with pRF or pR5UTRF along with either pcDNA3.1 or pcDNA3.1/HisB/TCP80. Twenty-four hours following the transfection, the cells were treated with or without etoposide for 2 hours. The cells were then lysed and a dual-luciferase assay was performed to detect firefly (Fluc) and renilla (Rluc) luciferase activities as described in Experimental procedures. The results presented are average ± SEM from three individual experiments.

    Journal: BioMed Research International

    Article Title: Translational Control Protein 80 Stimulates IRES-Mediated Translation of p53 mRNA in Response to DNA Damage

    doi: 10.1155/2015/708158

    Figure Lengend Snippet: (a) TCP80 has increased binding to the p53 mRNA following DNA damage. MCF-7 cells were transfected with pcDNA3.1/HisB/TCP80 that encodes for the Xpress-tagged TCP80 protein. Twenty-four hours following transfection, the cells were treated with or without 10 μ M etoposide for 2 hours. They were then lysed in polysome lysis buffer and incubated with protein G-plus agarose beads coated with the anti-Xpress antibody. The TCP80 and mRNA complexes (mRNP) were immunoprecipitated and mRNA was extracted from the immunoprecipitate as described in Experimental procedures. RT-PCR was then performed to reverse-transcribe and amplify the p53 IRES sequence (~145 bp). (b) TCP80 positively affects the p53 IRES activity in response to DNA damage. MCF-7 cells were cotransfected with pRF or pR5UTRF along with either pcDNA3.1 or pcDNA3.1/HisB/TCP80. Twenty-four hours following the transfection, the cells were treated with or without etoposide for 2 hours. The cells were then lysed and a dual-luciferase assay was performed to detect firefly (Fluc) and renilla (Rluc) luciferase activities as described in Experimental procedures. The results presented are average ± SEM from three individual experiments.

    Article Snippet: Materials Etoposide was from Calbiochem.

    Techniques: Binding Assay, Transfection, Lysis, Incubation, Immunoprecipitation, Reverse Transcription Polymerase Chain Reaction, Sequencing, Activity Assay, Luciferase

    The results of the MTS-based assay of cytotoxicity of sulfoxide 2a in the concentration range from 18 to 2.25 mM. Control is presented by 1.5% solution of ethyl alcohol. Cytostatic compound of comparison is etoposide (1.25 mM, Calbiochem, USA).

    Journal: Frontiers in Pharmacology

    Article Title: Sulfur-Containing Monoterpenoids as Potential Antithrombotic Drugs: Research in the Molecular Mechanism of Coagulation Activity Using Pinanyl Sulfoxide as an Example

    doi: 10.3389/fphar.2018.00116

    Figure Lengend Snippet: The results of the MTS-based assay of cytotoxicity of sulfoxide 2a in the concentration range from 18 to 2.25 mM. Control is presented by 1.5% solution of ethyl alcohol. Cytostatic compound of comparison is etoposide (1.25 mM, Calbiochem, USA).

    Article Snippet: Briefly, human BJ fibroblasts (ATCC, USA) were seeded in 96-well flat-bottomed plates (Corning Inc., Corning NY) and allowed to attach and grow for 24 h in complete medium DMEM/199 supplemented with 10% of fetal veal serum (FBS, GIBCO, GrandIsland, NY), L-glutamine (0,3 mg/ml) and antibiotics penicillin-streptomycin (Paneko, Russia), The cells were cultured at 37°C of 5% of CO2 (LamSystems, Russia) with the indicated concentrations of pinanylsulfoxide 2a, 1.5% solution of ethyl alcohol or chemotherapeutic agent etoposide (Calbiochem, USA) (control).

    Techniques: MTS Assay, Concentration Assay

    Etoposide induced p53 activity is dampened in chronic hypoxia. D283-MED cells were incubated in 1% O 2 or 21% O 2 for 1 day or 5 days, prior to etoposide treatment where indicated. Three p53 target genes, MDM2, PUMA and p21 were assessed by qPCR. ( a ) Basal levels of p53 target genes in hypoxia without etoposide treatment were measured. The mRNA levels were normalised with the house-keeping gene cyclophilin A. ( b ) Levels of MDM2, p21 and PUMA mRNA with or without etoposide treatment. Data represented as normalised to housekeeping gene (cyclophilin A) and fold change with respect to the untreated control. Data are representative of three independent experiments, error bars are SD of a single experiment. ( c ) Total p53 and phosphorylated p53 serine 15 levels assessed by western blot. ( d ) Densitometry quantification of the band intensity was analysed by ImageJ from 3 independent experiments. Plot represents p53 serine 15 over the p53 total

    Journal: BMC Cancer

    Article Title: Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in some brain tumour cells

    doi: 10.1186/s12885-019-5476-9

    Figure Lengend Snippet: Etoposide induced p53 activity is dampened in chronic hypoxia. D283-MED cells were incubated in 1% O 2 or 21% O 2 for 1 day or 5 days, prior to etoposide treatment where indicated. Three p53 target genes, MDM2, PUMA and p21 were assessed by qPCR. ( a ) Basal levels of p53 target genes in hypoxia without etoposide treatment were measured. The mRNA levels were normalised with the house-keeping gene cyclophilin A. ( b ) Levels of MDM2, p21 and PUMA mRNA with or without etoposide treatment. Data represented as normalised to housekeeping gene (cyclophilin A) and fold change with respect to the untreated control. Data are representative of three independent experiments, error bars are SD of a single experiment. ( c ) Total p53 and phosphorylated p53 serine 15 levels assessed by western blot. ( d ) Densitometry quantification of the band intensity was analysed by ImageJ from 3 independent experiments. Plot represents p53 serine 15 over the p53 total

    Article Snippet: Reagents Etoposide (E1383) was from Sigma.

    Techniques: Activity Assay, Incubation, Real-time Polymerase Chain Reaction, Western Blot

    Chronic hypoxia reduces ATM activation after etoposide treatment. D283-MED cells were pre-incubated in 21% O 2 , 1% O 2 or 0.1% O 2 prior to treatment with 20 μM etoposide for 4 h, or cells were left untreated as a control. Levels of ATM and ATM serine 1981 phosphorylation were determined using 3 independent western blots. The plots represent the densitometry of a representative western blot ( a ) measured using Image J

    Journal: BMC Cancer

    Article Title: Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in some brain tumour cells

    doi: 10.1186/s12885-019-5476-9

    Figure Lengend Snippet: Chronic hypoxia reduces ATM activation after etoposide treatment. D283-MED cells were pre-incubated in 21% O 2 , 1% O 2 or 0.1% O 2 prior to treatment with 20 μM etoposide for 4 h, or cells were left untreated as a control. Levels of ATM and ATM serine 1981 phosphorylation were determined using 3 independent western blots. The plots represent the densitometry of a representative western blot ( a ) measured using Image J

    Article Snippet: Reagents Etoposide (E1383) was from Sigma.

    Techniques: Activation Assay, Incubation, Western Blot

    Etoposide efficacy is not affected by hypoxia. D283-MED cells were incubated in 1% O 2 for 5 days or in 21% O 2 prior to etoposide (20 μM) treatment for indicated time points. ( a ) ɣH2AX bound secondary Cy3 antibodies were detected by immunofluorescence, staining intensity was quantified for individual cells using AQM analysis. Data shown are the mean ± S.E.M of three independent experiments ( n > 350 cells). One-way ANOVA followed by Bonferroni test was performed (*indicates p

    Journal: BMC Cancer

    Article Title: Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in some brain tumour cells

    doi: 10.1186/s12885-019-5476-9

    Figure Lengend Snippet: Etoposide efficacy is not affected by hypoxia. D283-MED cells were incubated in 1% O 2 for 5 days or in 21% O 2 prior to etoposide (20 μM) treatment for indicated time points. ( a ) ɣH2AX bound secondary Cy3 antibodies were detected by immunofluorescence, staining intensity was quantified for individual cells using AQM analysis. Data shown are the mean ± S.E.M of three independent experiments ( n > 350 cells). One-way ANOVA followed by Bonferroni test was performed (*indicates p

    Article Snippet: Reagents Etoposide (E1383) was from Sigma.

    Techniques: Incubation, Immunofluorescence, Staining

    Chronic hypoxia-induces treatment resistance in MB and glioblastoma cells. Cell viability was determined using an MTS assay, with absorbance normalised to untreated control. Two MB and one glioblastoma cell lines were pre-cultured in normoxia (21% O 2 ) or hypoxia (1% O 2 ) for the indicated time points prior to etoposide, cisplatin or X-ray irradiation treatment. Cells were maintained in 1% O 2 during etoposide [20–100 μM] and cisplatin [1–50 μg/ml] treatment. ( a ) D283-MED cells treated with etoposide ( b ) MEB-Med8A treated with etoposide ( c ) U87MG cells treated with etoposide. ( d ) D283-MED treated with cisplatin (1–5 μg/ml). ( e ) MEB-Med8A treated with cisplatin (1–5 μg/ml) ( f ) U87MG treated with cisplatin (30–50 μg/ml) ( g ) X-ray irradiation treatment was conducted in 21% O 2 with doses of 30 Gy (D283-MED), 50 Gy (MEB-Med8A) and 2 × 80 Gy dose (U87MG), with 48 h incubation post-treatment. The different doses is to account for different cell sensitivity to irradiation. Data are shown as the mean ± S.E.M of at least 3 independent experiments. A student t-test was performed where (*) indicates statistical significance with p

    Journal: BMC Cancer

    Article Title: Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in some brain tumour cells

    doi: 10.1186/s12885-019-5476-9

    Figure Lengend Snippet: Chronic hypoxia-induces treatment resistance in MB and glioblastoma cells. Cell viability was determined using an MTS assay, with absorbance normalised to untreated control. Two MB and one glioblastoma cell lines were pre-cultured in normoxia (21% O 2 ) or hypoxia (1% O 2 ) for the indicated time points prior to etoposide, cisplatin or X-ray irradiation treatment. Cells were maintained in 1% O 2 during etoposide [20–100 μM] and cisplatin [1–50 μg/ml] treatment. ( a ) D283-MED cells treated with etoposide ( b ) MEB-Med8A treated with etoposide ( c ) U87MG cells treated with etoposide. ( d ) D283-MED treated with cisplatin (1–5 μg/ml). ( e ) MEB-Med8A treated with cisplatin (1–5 μg/ml) ( f ) U87MG treated with cisplatin (30–50 μg/ml) ( g ) X-ray irradiation treatment was conducted in 21% O 2 with doses of 30 Gy (D283-MED), 50 Gy (MEB-Med8A) and 2 × 80 Gy dose (U87MG), with 48 h incubation post-treatment. The different doses is to account for different cell sensitivity to irradiation. Data are shown as the mean ± S.E.M of at least 3 independent experiments. A student t-test was performed where (*) indicates statistical significance with p

    Article Snippet: Reagents Etoposide (E1383) was from Sigma.

    Techniques: MTS Assay, Cell Culture, Irradiation, Incubation

    Etoposide and actinomycin D induced A3 expression and MT-COI editing in P2 cells. ( a ) Transcription profiling of A3A-A3H in etoposide or actinomycin D treated-P2 cells. Data in triplicate were normalized to the expression levels of RPL13A housekeeping reference genes and to untreated P2 cells to facilitate comparison (*p

    Journal: Scientific Reports

    Article Title: Genotoxic stress increases cytoplasmic mitochondrial DNA editing by human APOBEC3 mutator enzymes at a single cell level

    doi: 10.1038/s41598-019-39245-8

    Figure Lengend Snippet: Etoposide and actinomycin D induced A3 expression and MT-COI editing in P2 cells. ( a ) Transcription profiling of A3A-A3H in etoposide or actinomycin D treated-P2 cells. Data in triplicate were normalized to the expression levels of RPL13A housekeeping reference genes and to untreated P2 cells to facilitate comparison (*p

    Article Snippet: Reagents and Plasmids Etoposide was from Sigma and actinomycin D from Millipore.

    Techniques: Expressing

    Frequencies of A3-edited cymtDNA in single cells. Frequencies of single cells harboring A3-edited cymtDNA using a fixed PCR denaturation temperature of 85 °C. Analysis was performed in single CD4 + T lymphocytes from 2 donors D1 and D2, ~17% and 12% of cells scored positive for APOBEC3 edited cymtDNA. Among the 512 P2 ung − / − cells analyzed at 85 °C, 3 cells (0.6%) are positive. P2 ung − / − cells were treated with 100 μM actinomycin D (act D) or etoposide (etop) for 16 hours. Treatment increased the proportion of cells showing evidence of cymtDNA editing to ~24.6% and 22.2% with actinomycin D or etoposide respectively. f: frequency, #: number.

    Journal: Scientific Reports

    Article Title: Genotoxic stress increases cytoplasmic mitochondrial DNA editing by human APOBEC3 mutator enzymes at a single cell level

    doi: 10.1038/s41598-019-39245-8

    Figure Lengend Snippet: Frequencies of A3-edited cymtDNA in single cells. Frequencies of single cells harboring A3-edited cymtDNA using a fixed PCR denaturation temperature of 85 °C. Analysis was performed in single CD4 + T lymphocytes from 2 donors D1 and D2, ~17% and 12% of cells scored positive for APOBEC3 edited cymtDNA. Among the 512 P2 ung − / − cells analyzed at 85 °C, 3 cells (0.6%) are positive. P2 ung − / − cells were treated with 100 μM actinomycin D (act D) or etoposide (etop) for 16 hours. Treatment increased the proportion of cells showing evidence of cymtDNA editing to ~24.6% and 22.2% with actinomycin D or etoposide respectively. f: frequency, #: number.

    Article Snippet: Reagents and Plasmids Etoposide was from Sigma and actinomycin D from Millipore.

    Techniques: Polymerase Chain Reaction, Activated Clotting Time Assay

    Flow cytometry (FACS analysis) of Jurkat cells treated with ( a ) 0.5 μ M staurosporine or ( b ) 50 μ M etoposide. In ( c ), treatments for 24 h were (1) 10 μ M rapamycin; (2) 50 μ M etoposide; (3) 50 μ M etoposide plus pan caspase inhibitor z-VAD-fmk; (4) 15 ng/ml TRAIL; (5) 15 ng/ml TRAIL plus z-VAD-fmk; (6) untreated. ( a – c ) ■, Annexin V-positive; ■, Annexin V-positive and mAb2C4:AF568-positive; ■, mAb2C4:AF568-positive and ■; double-negative, viable cells.

    Journal: Cell Death Discovery

    Article Title: A novel ligand of calcitonin receptor reveals a potential new sensor that modulates programmed cell death

    doi: 10.1038/cddiscovery.2016.62

    Figure Lengend Snippet: Flow cytometry (FACS analysis) of Jurkat cells treated with ( a ) 0.5 μ M staurosporine or ( b ) 50 μ M etoposide. In ( c ), treatments for 24 h were (1) 10 μ M rapamycin; (2) 50 μ M etoposide; (3) 50 μ M etoposide plus pan caspase inhibitor z-VAD-fmk; (4) 15 ng/ml TRAIL; (5) 15 ng/ml TRAIL plus z-VAD-fmk; (6) untreated. ( a – c ) ■, Annexin V-positive; ■, Annexin V-positive and mAb2C4:AF568-positive; ■, mAb2C4:AF568-positive and ■; double-negative, viable cells.

    Article Snippet: Other cytotoxins used included 50 μ M etoposide (Sigma Aldrich), 10 μ M rapamycin (VETRANAL, Sigma Aldrich) and 15 ng/ml TRAIL (Abcam, Cambridge, UK) sometimes in combination with the pan-caspase inhibitor 5 μ g/ml z-VAD-fms (Santa Cruz, Dallas, TX, USA).

    Techniques: Flow Cytometry, Cytometry, FACS

    MG63 cells were treated with cytotoxins for 19 h to induce PCD. Live staining with mAb2C4:AF568 and annexin V:AF488, was followed by fixation and staining with additional primary antibodies (caspase 8, LC3B or α -tubulin) followed by specific species or isotype secondary antibody:AlexaFluors. ( a – d ) MG63 cells were treated with 1 μ M staurosporine: ( a ), a merged image, with arrows indicating examples of nuclei from unaffected cells; ( b ) mAb2C4:AF568; ( c ) annexin V:AF488; and ( d ) cleaved caspase 8. ( e and f ) merged images of MG63 cells were treated with 50 μ M etoposide+30 μ M necrostatin-1 (DAPI (4,6-diamidino-2-phenylindole), blue; mAb2C4:AF568, red; annexin V:AF488, green). ( g and h ) mAb2C4:AF568 (red channel) and merged image of MG63 cells treated with 50 μ M chloroquine to induce autophagy (DAPI, blue; mAb2C4:AF568, red; LC3B, green). ( i and j ) MG63 cells treated with tumor necrosis factor α and zVAD-fms underwent necroptosis (mAb2C4:AF568, red; annexin V, green). ( k ) MG63 cells were untreated as controls (DAPI, blue; α -tubulin, green). ( l – p ) MG63 cells were treated with 1% DMSO+1 μ M paclitaxel: ( l , DAPI, blue; α -tubulin, green; mAb2C4:AF568, red) induced into the PACSR. ( q – t ) separate experiment with cells treated with 1% DMSO+1 μ M paclitaxel: (DAPI, blue; mAb2C4:AF568, red; α -tubulin, pseudo-green) The calibration bar shown in ( t ) represents ( a – e , k and l ) 25 μ m and ( f – j , m - t ) 10 μ m.

    Journal: Cell Death Discovery

    Article Title: A novel ligand of calcitonin receptor reveals a potential new sensor that modulates programmed cell death

    doi: 10.1038/cddiscovery.2016.62

    Figure Lengend Snippet: MG63 cells were treated with cytotoxins for 19 h to induce PCD. Live staining with mAb2C4:AF568 and annexin V:AF488, was followed by fixation and staining with additional primary antibodies (caspase 8, LC3B or α -tubulin) followed by specific species or isotype secondary antibody:AlexaFluors. ( a – d ) MG63 cells were treated with 1 μ M staurosporine: ( a ), a merged image, with arrows indicating examples of nuclei from unaffected cells; ( b ) mAb2C4:AF568; ( c ) annexin V:AF488; and ( d ) cleaved caspase 8. ( e and f ) merged images of MG63 cells were treated with 50 μ M etoposide+30 μ M necrostatin-1 (DAPI (4,6-diamidino-2-phenylindole), blue; mAb2C4:AF568, red; annexin V:AF488, green). ( g and h ) mAb2C4:AF568 (red channel) and merged image of MG63 cells treated with 50 μ M chloroquine to induce autophagy (DAPI, blue; mAb2C4:AF568, red; LC3B, green). ( i and j ) MG63 cells treated with tumor necrosis factor α and zVAD-fms underwent necroptosis (mAb2C4:AF568, red; annexin V, green). ( k ) MG63 cells were untreated as controls (DAPI, blue; α -tubulin, green). ( l – p ) MG63 cells were treated with 1% DMSO+1 μ M paclitaxel: ( l , DAPI, blue; α -tubulin, green; mAb2C4:AF568, red) induced into the PACSR. ( q – t ) separate experiment with cells treated with 1% DMSO+1 μ M paclitaxel: (DAPI, blue; mAb2C4:AF568, red; α -tubulin, pseudo-green) The calibration bar shown in ( t ) represents ( a – e , k and l ) 25 μ m and ( f – j , m - t ) 10 μ m.

    Article Snippet: Other cytotoxins used included 50 μ M etoposide (Sigma Aldrich), 10 μ M rapamycin (VETRANAL, Sigma Aldrich) and 15 ng/ml TRAIL (Abcam, Cambridge, UK) sometimes in combination with the pan-caspase inhibitor 5 μ g/ml z-VAD-fms (Santa Cruz, Dallas, TX, USA).

    Techniques: Staining

    Inhibition of RAD51 expression and Etoposide induces apoptosis in sphere cultures. (a) HeLa SPhere culture was exposed to 30 nM of siRAD51 and 5.8 μ g/mL of VP16. By MTT assay, cell viability was affected in the presence of both compounds, but not when they were added independently. The absence of RAD51 protein decreased the cell viability of spheres exposed to VP16. HeLa SP culture exposed to VP16 and 30 nM of random siRNA (scrambled) was used as control. (b and c) Apoptosis was evaluated by Annexin-V assay (see Materials and Methods) under identical conditions; the highest level of apoptosis was exhibited in the presence of both VP16 and siRAD51. The absence of RAD51 protein sensitized spheres to VP16. (d and e) Control indicating that treatment with siRAD51 and Etoposide induces apoptosis in ML cells. ∗∗ p

    Journal: Stem Cells International

    Article Title: Inhibition of RAD51 by siRNA and Resveratrol Sensitizes Cancer Stem Cells Derived from HeLa Cell Cultures to Apoptosis

    doi: 10.1155/2018/2493869

    Figure Lengend Snippet: Inhibition of RAD51 expression and Etoposide induces apoptosis in sphere cultures. (a) HeLa SPhere culture was exposed to 30 nM of siRAD51 and 5.8 μ g/mL of VP16. By MTT assay, cell viability was affected in the presence of both compounds, but not when they were added independently. The absence of RAD51 protein decreased the cell viability of spheres exposed to VP16. HeLa SP culture exposed to VP16 and 30 nM of random siRNA (scrambled) was used as control. (b and c) Apoptosis was evaluated by Annexin-V assay (see Materials and Methods) under identical conditions; the highest level of apoptosis was exhibited in the presence of both VP16 and siRAD51. The absence of RAD51 protein sensitized spheres to VP16. (d and e) Control indicating that treatment with siRAD51 and Etoposide induces apoptosis in ML cells. ∗∗ p

    Article Snippet: RESveratrol (RES) (trans-3,4′,5-trihydroxystilbene; > 99% pure) (Sigma, 5010) was dissolved in ethanol at 80 mM and stored at −20°C; when used, it was diluted with Dulbecco's modified Eagle's medium (DMEM) to a final concentration of 137 μ M; Etoposide (VP16) (Sigma, 33419-42-0) stock solution was prepared at 500 mg/mL in phosphate buffer saline (PBS) and diluted with DMEM to the final concentration of 5.8 μ g/mL (10 μ M).

    Techniques: Inhibition, Expressing, MTT Assay, Annexin V Assay

    Inhibition of RAD51 decreases cell viability. (a) Western blot analysis showing RAD51 is overexpressed in HeLa SP cultures compared to the monolayer ones. (b) RAD51 expression is induced by Etoposide and efficiently inhibited by siRNA targeted to RAD51 (siRAD51). Western blot analysis shows that RAD51 expression is inhibited by increased amounts of siRAD51 (5, 10, 20, and 30 nM) in the presence of 5.8 μ g/mL of VP16 for 48 h. (c) Inhibition of RAD51 expression in sphere culture sensitizes to VP16. Cell viability of spheres measured by MTT decreases with increasing concentrations of siRAD51 in the presence of VP16. ∗∗∗ p

    Journal: Stem Cells International

    Article Title: Inhibition of RAD51 by siRNA and Resveratrol Sensitizes Cancer Stem Cells Derived from HeLa Cell Cultures to Apoptosis

    doi: 10.1155/2018/2493869

    Figure Lengend Snippet: Inhibition of RAD51 decreases cell viability. (a) Western blot analysis showing RAD51 is overexpressed in HeLa SP cultures compared to the monolayer ones. (b) RAD51 expression is induced by Etoposide and efficiently inhibited by siRNA targeted to RAD51 (siRAD51). Western blot analysis shows that RAD51 expression is inhibited by increased amounts of siRAD51 (5, 10, 20, and 30 nM) in the presence of 5.8 μ g/mL of VP16 for 48 h. (c) Inhibition of RAD51 expression in sphere culture sensitizes to VP16. Cell viability of spheres measured by MTT decreases with increasing concentrations of siRAD51 in the presence of VP16. ∗∗∗ p

    Article Snippet: RESveratrol (RES) (trans-3,4′,5-trihydroxystilbene; > 99% pure) (Sigma, 5010) was dissolved in ethanol at 80 mM and stored at −20°C; when used, it was diluted with Dulbecco's modified Eagle's medium (DMEM) to a final concentration of 137 μ M; Etoposide (VP16) (Sigma, 33419-42-0) stock solution was prepared at 500 mg/mL in phosphate buffer saline (PBS) and diluted with DMEM to the final concentration of 5.8 μ g/mL (10 μ M).

    Techniques: Inhibition, Western Blot, Expressing, MTT Assay

    HeLa SPheres are resistant to the effects of Etoposide. HeLa SPhere and MonoLayer cultures were treated for 24 h with 5.8 μ g/mL of VP16. (a) Flow cytometry graphic showing Annexin-V assay in SPhere (SP) and MonoLayer (ML) cultures. (b) Graphic shows that apoptosis percentage was higher in ML cells than in SP cultures. (c) Etoposide (VP16) has no effect on SP culture viability but drastically reduces the cell viability of ML cultures. Cell viability evaluated by MTT assay (see Materials and Methods) shows that SP are more resistant to VP16 treatment than ML. ∗∗∗ p

    Journal: Stem Cells International

    Article Title: Inhibition of RAD51 by siRNA and Resveratrol Sensitizes Cancer Stem Cells Derived from HeLa Cell Cultures to Apoptosis

    doi: 10.1155/2018/2493869

    Figure Lengend Snippet: HeLa SPheres are resistant to the effects of Etoposide. HeLa SPhere and MonoLayer cultures were treated for 24 h with 5.8 μ g/mL of VP16. (a) Flow cytometry graphic showing Annexin-V assay in SPhere (SP) and MonoLayer (ML) cultures. (b) Graphic shows that apoptosis percentage was higher in ML cells than in SP cultures. (c) Etoposide (VP16) has no effect on SP culture viability but drastically reduces the cell viability of ML cultures. Cell viability evaluated by MTT assay (see Materials and Methods) shows that SP are more resistant to VP16 treatment than ML. ∗∗∗ p

    Article Snippet: RESveratrol (RES) (trans-3,4′,5-trihydroxystilbene; > 99% pure) (Sigma, 5010) was dissolved in ethanol at 80 mM and stored at −20°C; when used, it was diluted with Dulbecco's modified Eagle's medium (DMEM) to a final concentration of 137 μ M; Etoposide (VP16) (Sigma, 33419-42-0) stock solution was prepared at 500 mg/mL in phosphate buffer saline (PBS) and diluted with DMEM to the final concentration of 5.8 μ g/mL (10 μ M).

    Techniques: Flow Cytometry, Cytometry, Annexin V Assay, MTT Assay

    Resveratrol inhibits RAD51 expression in sphere cultures. (a) VP16 in the presence of RESveratrol (RES) decreases cell viability in HeLa SPhere (SP) cultures. Culture was exposed 72 h to both 5.8 μ g/mL VP16 and 137 μ M RES. Under these conditions, cell viability measured by MTT assay was strongly decreased (to 15.3%). Ethanol was used as vehicle control. (b) Western blot analysis shows that RES (137 μ M) treatment for 48 h inhibited RAD51 protein expression (similar to siRAD51) in SP cultures as compared to HeLa SP without treatment or HeLa SP treated with Etoposide. RAD51 protein levels were highly reduced when HeLa SP were treated with resveratrol alone or together with Etoposide. Untreated MonoLayer (ML) HeLa cells were also used as a control.

    Journal: Stem Cells International

    Article Title: Inhibition of RAD51 by siRNA and Resveratrol Sensitizes Cancer Stem Cells Derived from HeLa Cell Cultures to Apoptosis

    doi: 10.1155/2018/2493869

    Figure Lengend Snippet: Resveratrol inhibits RAD51 expression in sphere cultures. (a) VP16 in the presence of RESveratrol (RES) decreases cell viability in HeLa SPhere (SP) cultures. Culture was exposed 72 h to both 5.8 μ g/mL VP16 and 137 μ M RES. Under these conditions, cell viability measured by MTT assay was strongly decreased (to 15.3%). Ethanol was used as vehicle control. (b) Western blot analysis shows that RES (137 μ M) treatment for 48 h inhibited RAD51 protein expression (similar to siRAD51) in SP cultures as compared to HeLa SP without treatment or HeLa SP treated with Etoposide. RAD51 protein levels were highly reduced when HeLa SP were treated with resveratrol alone or together with Etoposide. Untreated MonoLayer (ML) HeLa cells were also used as a control.

    Article Snippet: RESveratrol (RES) (trans-3,4′,5-trihydroxystilbene; > 99% pure) (Sigma, 5010) was dissolved in ethanol at 80 mM and stored at −20°C; when used, it was diluted with Dulbecco's modified Eagle's medium (DMEM) to a final concentration of 137 μ M; Etoposide (VP16) (Sigma, 33419-42-0) stock solution was prepared at 500 mg/mL in phosphate buffer saline (PBS) and diluted with DMEM to the final concentration of 5.8 μ g/mL (10 μ M).

    Techniques: Expressing, MTT Assay, Western Blot

    GDNF and VP-16 expression patterns . The GDNF expression pattern of the final ON group ( a , b ) was similar to that previously observed where the GDNF transgene (red) is observed distally from that of the transduced cells and VP-16 (green). ( b ) Increased magnification of area outlined in a . VP-16 expression in the OFF group ( c , d ) was similar to that seen in the ON group; however, no GDNF protein expression was observed. GDNF protein expression in the CBA-GDNF group ( e , f ) extended in a diffuse pattern into the VTA and the DMN indicating that GDNF protein was distributed away from the transduced cells in contrast to the pattern of expression observed from an intracellular transgene such as the SN-GFP group ( g , h ). As expected, no immunoreactivity was observed for VP-16 in either the CBA-GDNF group ( e , f , green) or the SN-GFP group ( g , h , red). ( f and h ) Higher magnifications of areas outlined in e and g , respectively. Bar: a , c , e , g = 1.0 mm, bar: b , d , f , h = 0.1 mm. CBA, chicken β-actin; DMN, deep mesencephalic nucleus; GDNF, glial cell line-derived neurotrophic factor; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulate; VTA, ventral tegmental area.

    Journal: Molecular Therapy

    Article Title: Tight Long-term Dynamic Doxycycline Responsive Nigrostriatal GDNF Using a Single rAAV Vector

    doi: 10.1038/mt.2009.196

    Figure Lengend Snippet: GDNF and VP-16 expression patterns . The GDNF expression pattern of the final ON group ( a , b ) was similar to that previously observed where the GDNF transgene (red) is observed distally from that of the transduced cells and VP-16 (green). ( b ) Increased magnification of area outlined in a . VP-16 expression in the OFF group ( c , d ) was similar to that seen in the ON group; however, no GDNF protein expression was observed. GDNF protein expression in the CBA-GDNF group ( e , f ) extended in a diffuse pattern into the VTA and the DMN indicating that GDNF protein was distributed away from the transduced cells in contrast to the pattern of expression observed from an intracellular transgene such as the SN-GFP group ( g , h ). As expected, no immunoreactivity was observed for VP-16 in either the CBA-GDNF group ( e , f , green) or the SN-GFP group ( g , h , red). ( f and h ) Higher magnifications of areas outlined in e and g , respectively. Bar: a , c , e , g = 1.0 mm, bar: b , d , f , h = 0.1 mm. CBA, chicken β-actin; DMN, deep mesencephalic nucleus; GDNF, glial cell line-derived neurotrophic factor; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulate; VTA, ventral tegmental area.

    Article Snippet: Primary antibodies used were mouse anti-TH (1:2,000), rabbit anti-GFP (1:2,000), mouse anti-calbindin (1:200), rabbit anti-VP-16 (1:50) (Chemicon, Temecula, CA), goat anti-GDNF (1:1,000) (R & D Systems, Minneapolis, MN).

    Techniques: Expressing, Crocin Bleaching Assay, Derivative Assay

    Experimental design and vector schematics . rAAV genomic maps of vectors used in all three experiments. ( a ) CBA-GDNF, ( b ) CBA-GFP, and ( c ) regGDNF. ( d ) Experimental design and timeline of the three experiments performed in this study. The alternating white gray areas indicate the crossover of feeding DOX or normal food in the ON–OFF experiment. At the end of the ON–OFF study, SN-regGDNF1 was in the OFF state (expressing GDNF) and SN-regGDNF2 was in the ON state. The different shades of gray in the dose–response experiment denote the fact that the DOX diet doses were changed during that experiment as indicated. No DOX was administered during the striatum experiment. ( e ) Photograph of the ventral surface of the rat brain displaying how the brain was divided for the assays and histology as described. CMVe, cytomegalovirus enhancer element; DOX, doxycycline; eGFP, enhanced green fluorescent protein; hGDNF, human glial cell line-derived neurotrophic factor; iTR, inverted terminal repeat; pCBA, chicken β-actin promoter; pTET-dCMV minimal , tetracycline-responsive delta-CMV minimal promoter; rAAV, recombinant adeno-associated virus; SV40 pA, SV40 poly-A sequence; tTA2, transactivator containing VP-16 sequence.

    Journal: Molecular Therapy

    Article Title: Tight Long-term Dynamic Doxycycline Responsive Nigrostriatal GDNF Using a Single rAAV Vector

    doi: 10.1038/mt.2009.196

    Figure Lengend Snippet: Experimental design and vector schematics . rAAV genomic maps of vectors used in all three experiments. ( a ) CBA-GDNF, ( b ) CBA-GFP, and ( c ) regGDNF. ( d ) Experimental design and timeline of the three experiments performed in this study. The alternating white gray areas indicate the crossover of feeding DOX or normal food in the ON–OFF experiment. At the end of the ON–OFF study, SN-regGDNF1 was in the OFF state (expressing GDNF) and SN-regGDNF2 was in the ON state. The different shades of gray in the dose–response experiment denote the fact that the DOX diet doses were changed during that experiment as indicated. No DOX was administered during the striatum experiment. ( e ) Photograph of the ventral surface of the rat brain displaying how the brain was divided for the assays and histology as described. CMVe, cytomegalovirus enhancer element; DOX, doxycycline; eGFP, enhanced green fluorescent protein; hGDNF, human glial cell line-derived neurotrophic factor; iTR, inverted terminal repeat; pCBA, chicken β-actin promoter; pTET-dCMV minimal , tetracycline-responsive delta-CMV minimal promoter; rAAV, recombinant adeno-associated virus; SV40 pA, SV40 poly-A sequence; tTA2, transactivator containing VP-16 sequence.

    Article Snippet: Primary antibodies used were mouse anti-TH (1:2,000), rabbit anti-GFP (1:2,000), mouse anti-calbindin (1:200), rabbit anti-VP-16 (1:50) (Chemicon, Temecula, CA), goat anti-GDNF (1:1,000) (R & D Systems, Minneapolis, MN).

    Techniques: Plasmid Preparation, Crocin Bleaching Assay, Expressing, Derivative Assay, Recombinant, Sequencing

    Effects of engraftment location, estrogen, and immune suppressant on tumorigenicity of breast cancer cells NOD/SCID mice were treated ± 17β-estradiol (E 2 ) and etoposide as indicated. Six days later, mice were surgically incised and injected with 500 cells from a breast cancer pleural effusion in 25% Matrigel. A: final tumor volume. Data represent mean ± SE. B: tumor incidence. C: latency of tumor formation following injection (* P

    Journal: Journal of cellular physiology

    Article Title: Local regulation of human breast xenograft models

    doi: 10.1002/jcp.22190

    Figure Lengend Snippet: Effects of engraftment location, estrogen, and immune suppressant on tumorigenicity of breast cancer cells NOD/SCID mice were treated ± 17β-estradiol (E 2 ) and etoposide as indicated. Six days later, mice were surgically incised and injected with 500 cells from a breast cancer pleural effusion in 25% Matrigel. A: final tumor volume. Data represent mean ± SE. B: tumor incidence. C: latency of tumor formation following injection (* P

    Article Snippet: Six days prior to cell injection, mice were treated ± subcutaneous 17β-estradiol pellet (0.72 mg, 90-day release; Innovative Research of America, Sarasota, FL) and ± the bone marrow suppressant VP-16 (etoposide, a commonly used immune suppressant, 0.6 mg; Calbiochem, Gibbstown, NJ) administered i.p. ( ; ; ).

    Techniques: Mouse Assay, Injection

    MMS22L foci form during S phase of the cell cycle and colocalize with HR proteins Immunofluorescence images of MMS22L foci formation at etoposide (ETP)‐induced DSBs during S, M, and G1 phases of the cell cycle in HeLa cells. Scale bar: 5 μm. Quantification of a representative experiment from (A) shows number of MMS22L foci per nucleus during indicated cell cycle phases ( n = 2; n nuclei ≥ 60). Immunofluorescence images of CPT‐induced MMS22L, RPA2, BRCA2, and RAD51 foci in U2OS cells. Scale bar: 5 μm. Quantification of a representative experiment ( n = 3) from (C) shows percentage of γH2AX, RPA2, BRCA2, and RAD51 foci colocalizing with MMS22L foci ( n nuclei = 30; nuclei with ≥ 25 MMS22L foci were analyzed). Data information: Boxplots in (B and D) represent distributions per nucleus; boxes indicate the 25–75 percentile and whiskers the 10–90 percentile. Horizontal lines mark the medians. Statistical analysis: Mann–Whitney U ‐test; *** P ≤ 0.0001; ns, not significant.

    Journal: The EMBO Journal

    Article Title: The MMS22L–TONSL heterodimer directly promotes RAD51‐dependent recombination upon replication stress

    doi: 10.15252/embj.201593132

    Figure Lengend Snippet: MMS22L foci form during S phase of the cell cycle and colocalize with HR proteins Immunofluorescence images of MMS22L foci formation at etoposide (ETP)‐induced DSBs during S, M, and G1 phases of the cell cycle in HeLa cells. Scale bar: 5 μm. Quantification of a representative experiment from (A) shows number of MMS22L foci per nucleus during indicated cell cycle phases ( n = 2; n nuclei ≥ 60). Immunofluorescence images of CPT‐induced MMS22L, RPA2, BRCA2, and RAD51 foci in U2OS cells. Scale bar: 5 μm. Quantification of a representative experiment ( n = 3) from (C) shows percentage of γH2AX, RPA2, BRCA2, and RAD51 foci colocalizing with MMS22L foci ( n nuclei = 30; nuclei with ≥ 25 MMS22L foci were analyzed). Data information: Boxplots in (B and D) represent distributions per nucleus; boxes indicate the 25–75 percentile and whiskers the 10–90 percentile. Horizontal lines mark the medians. Statistical analysis: Mann–Whitney U ‐test; *** P ≤ 0.0001; ns, not significant.

    Article Snippet: Cells were treated with the following drugs diluted in growth medium: Topo II inhibitor etoposide (5 μM; Sigma‐Aldrich), Topo I inhibitor camptothecin (Sigma‐Aldrich), hydroxyurea (Sigma‐Aldrich), polymerase‐alpha inhibitor aphidicolin (2 μM; Sigma‐Aldrich), and ATR inhibitor VE‐821 (3 μM; Selleck Chemicals).

    Techniques: Immunofluorescence, Cycling Probe Technology, MANN-WHITNEY

    Precise quantification of individual treatment effects and monitoring of distinct clinical stages. a Imaging visualizes treatment-induced cell loss and regrowth; 10 5 ALL-50 cells/mouse were injected into 10 mice which received a single intraperitoneal dose of Etoposid (VP-16; 50 mg/kg) in week 6 after tumor cell injection, except the control mouse which was treated with PBS. Animals were imaged before treatment (pre-treatment) and 4 and 11 days after treatment; shown is one representative mouse; all mice are shown in Supplemental Figure 11; b, c Imaging visualizes different sensitivities of individual samples towards treatment; ALL-199 (1×10 4 cells/mouse) or ALL-4S (5×10 4 cells/mouse) were injected into 16 mice; mice were randomized in week 4 into one control (n = 4) and two experimental groups (n = 6 each). Control mice received buffer injection, while the other groups were treated once intraperitoneally with either Etoposid (VP-16; 50 mg/kg) or cyclophosphamide (Cyclo; 150 mg/kg) as indicated. Mice were imaged directly before and 4 days after treatment; shown are 3 representative mice of each treatment group before and 4 days after treatment ( b ); shown is the result of quantification of the images; each line represents a single mouse ( c ); * P

    Journal: PLoS ONE

    Article Title: In Vivo Imaging Enables High Resolution Preclinical Trials on Patients' Leukemia Cells Growing in Mice

    doi: 10.1371/journal.pone.0052798

    Figure Lengend Snippet: Precise quantification of individual treatment effects and monitoring of distinct clinical stages. a Imaging visualizes treatment-induced cell loss and regrowth; 10 5 ALL-50 cells/mouse were injected into 10 mice which received a single intraperitoneal dose of Etoposid (VP-16; 50 mg/kg) in week 6 after tumor cell injection, except the control mouse which was treated with PBS. Animals were imaged before treatment (pre-treatment) and 4 and 11 days after treatment; shown is one representative mouse; all mice are shown in Supplemental Figure 11; b, c Imaging visualizes different sensitivities of individual samples towards treatment; ALL-199 (1×10 4 cells/mouse) or ALL-4S (5×10 4 cells/mouse) were injected into 16 mice; mice were randomized in week 4 into one control (n = 4) and two experimental groups (n = 6 each). Control mice received buffer injection, while the other groups were treated once intraperitoneally with either Etoposid (VP-16; 50 mg/kg) or cyclophosphamide (Cyclo; 150 mg/kg) as indicated. Mice were imaged directly before and 4 days after treatment; shown are 3 representative mice of each treatment group before and 4 days after treatment ( b ); shown is the result of quantification of the images; each line represents a single mouse ( c ); * P

    Article Snippet: Preclinical in vivo Treatment Trials Control animals received physiological salt solution intraperitoneally; treatment group mice were injected i.p. with a single dose of either Etoposid (VP-16; 50 mg/kg; Sigma, Hamburg, Germany) or Cyclophosphamide (Cyclo; 150 mg/kg; Baxter, Unterschleissheim, Germany) diluted in 0.9% NaCl.

    Techniques: Imaging, Injection, Mouse Assay