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s8592 e7449 stenoparib selleckchem  (Selleck Chemicals)


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    Selleck Chemicals s8592 e7449 stenoparib selleckchem
    Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) <t>E7449,</t> (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.
    S8592 E7449 Stenoparib Selleckchem, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 92/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells."

    Article Title: A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells.

    Journal: Cell reports

    doi: 10.1016/j.celrep.2024.114234

    Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.
    Figure Legend Snippet: Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.

    Techniques Used:

    Figure 3. Exchange rates of PARP1 at DNA damage sites upon PARPi (A–G) NormalizedexchangeratesofPARP1 atIR-inducedDNA damage sites following treatmentwith(A) pamiparib,(B) veliparib, (C)olaparib, (D)rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the FRAP half-times of PARP1 DNA repair foci estimated via FRAP modeling. Red dots indicate the mean value. (H) PTC values calculated based on the mean FRAP half-times of PARP1 repair foci. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figures S3 and S6.
    Figure Legend Snippet: Figure 3. Exchange rates of PARP1 at DNA damage sites upon PARPi (A–G) NormalizedexchangeratesofPARP1 atIR-inducedDNA damage sites following treatmentwith(A) pamiparib,(B) veliparib, (C)olaparib, (D)rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the FRAP half-times of PARP1 DNA repair foci estimated via FRAP modeling. Red dots indicate the mean value. (H) PTC values calculated based on the mean FRAP half-times of PARP1 repair foci. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figures S3 and S6.

    Techniques Used:

    Figure 4. Kinetics of ARH3 at DNA damage sites upon PARPi (A–G) Kinetics of recruitment and removal of ARH3 at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the maximum total fluorescence intensity of ARH3 at DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PIC values calculated based on the mean maximum fluorescence intensity of ARH3 at DNA damage sites. (I) PARP1 residual activities and in vivo IC50 values. Error bars represent the SD. NT, no treatment; CI, confidence interval; n.d., not determined. See also Fig- ure S4.
    Figure Legend Snippet: Figure 4. Kinetics of ARH3 at DNA damage sites upon PARPi (A–G) Kinetics of recruitment and removal of ARH3 at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the maximum total fluorescence intensity of ARH3 at DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PIC values calculated based on the mean maximum fluorescence intensity of ARH3 at DNA damage sites. (I) PARP1 residual activities and in vivo IC50 values. Error bars represent the SD. NT, no treatment; CI, confidence interval; n.d., not determined. See also Fig- ure S4.

    Techniques Used: In Vivo

    Figure 6. PARPis rearrange downstream DNA repair events (A) Correlations between the average half-times of recruitment of RFC4, PCNA, POLD2, and POLH following PARPi and PRC values for evaluated PARPis. Error bars represent the SD. (B) Correlation between the extent of uncoupling of PCNA removal and RPA1 recruitment and PRC values for evaluated PARPis. The uncoupling is calculated as the average difference between the half-times of removal of PCNA and the half-times of recruitment of RPA1 at the single-cell level. Ruca- and niraparib have been removed from the correlation graph on the right as outliers. Error bars represent the SD. (C) Clonogenic assay of HeLa Kyoto cells treated with the indicated PARPi concentrations. (D) Mean surviving fractions ± SEM of HeLa Kyoto cells treated with the indicated PARPi concentrations (n = 3). (E) Cell viability IC50 values (half-maximal suppression of cell viability). Error bars represent the SEM. White dots indicate the mean value. P, pamiparib; V, ve- liparib; O, olaparib; R, rucaparib; E, E7449; N, niraparib; T, talazoparib; n.d., not determined. See also Figure S7.
    Figure Legend Snippet: Figure 6. PARPis rearrange downstream DNA repair events (A) Correlations between the average half-times of recruitment of RFC4, PCNA, POLD2, and POLH following PARPi and PRC values for evaluated PARPis. Error bars represent the SD. (B) Correlation between the extent of uncoupling of PCNA removal and RPA1 recruitment and PRC values for evaluated PARPis. The uncoupling is calculated as the average difference between the half-times of removal of PCNA and the half-times of recruitment of RPA1 at the single-cell level. Ruca- and niraparib have been removed from the correlation graph on the right as outliers. Error bars represent the SD. (C) Clonogenic assay of HeLa Kyoto cells treated with the indicated PARPi concentrations. (D) Mean surviving fractions ± SEM of HeLa Kyoto cells treated with the indicated PARPi concentrations (n = 3). (E) Cell viability IC50 values (half-maximal suppression of cell viability). Error bars represent the SEM. White dots indicate the mean value. P, pamiparib; V, ve- liparib; O, olaparib; R, rucaparib; E, E7449; N, niraparib; T, talazoparib; n.d., not determined. See also Figure S7.

    Techniques Used: Clonogenic Assay



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    Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) <t>E7449,</t> (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.
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    Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.

    Journal: Cell reports

    Article Title: A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells.

    doi: 10.1016/j.celrep.2024.114234

    Figure Lengend Snippet: Figure 2. Kinetics of PARP1 at DNA damage sites upon PARPi (A–G) Normalized kinetics of PARP1 recruitment and removal at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict half-times of PARP1 removal from DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PRC values calculated based on the mean half-times of PARP1 removal from DNA damage sites. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figure S2.

    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Chemicals, peptides, and recombinant proteins FluoroBrite DMEM Thermo Fisher Scientific Cat# A1896701 GlutaMAX Supplement Thermo Fisher Scientific Cat# 35050061 BMN673 (Talazoparib) Selleckchem Cat# S7048 AZD5305 (Saruparib) Selleckchem Cat# S9875 Rucaparib Selleckchem Cat# S4948 Niraparib (MK-4827) Selleckchem Cat# S2741 Veliparib Selleckchem Cat# S1004 Pamiparib Selleckchem Cat# S8592 E7449 (Stenoparib) Selleckchem Cat# S8419 A-966492 Selleckchem Cat# S2197 Olaparib (AZD2281) Selleckchem Cat# S1060 Experimental models: Cell lines Human: HeLa Kyoto ATCC CRL-11268; RRID:CVCL_1922 Human: HeLa Kyoto RFC4-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto PARP1-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto POLD2-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto POLH-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto RPA1-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto ADPRHL2-LAP cells The Hyman Laboratory, MPI-CBG 8494 Human: DLD1 Cell line Horizon Discovery Cat# HD 105-027; RRID:CVCL_0248 Human: DLD1 PARP1-LAP This paper N/A Human: PC3 Cell line RRID:CVCL_0035 Human: PC3 PARP1-LAP This paper N/A Software and algorithms CellTool Danovski et al.40 https://dnarepair.bas.bg/software/CellTool/

    Techniques:

    Figure 3. Exchange rates of PARP1 at DNA damage sites upon PARPi (A–G) NormalizedexchangeratesofPARP1 atIR-inducedDNA damage sites following treatmentwith(A) pamiparib,(B) veliparib, (C)olaparib, (D)rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the FRAP half-times of PARP1 DNA repair foci estimated via FRAP modeling. Red dots indicate the mean value. (H) PTC values calculated based on the mean FRAP half-times of PARP1 repair foci. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figures S3 and S6.

    Journal: Cell reports

    Article Title: A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells.

    doi: 10.1016/j.celrep.2024.114234

    Figure Lengend Snippet: Figure 3. Exchange rates of PARP1 at DNA damage sites upon PARPi (A–G) NormalizedexchangeratesofPARP1 atIR-inducedDNA damage sites following treatmentwith(A) pamiparib,(B) veliparib, (C)olaparib, (D)rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the FRAP half-times of PARP1 DNA repair foci estimated via FRAP modeling. Red dots indicate the mean value. (H) PTC values calculated based on the mean FRAP half-times of PARP1 repair foci. Error bars represent the SD. NT, no treatment; n.d., not determined. See also Figures S3 and S6.

    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Chemicals, peptides, and recombinant proteins FluoroBrite DMEM Thermo Fisher Scientific Cat# A1896701 GlutaMAX Supplement Thermo Fisher Scientific Cat# 35050061 BMN673 (Talazoparib) Selleckchem Cat# S7048 AZD5305 (Saruparib) Selleckchem Cat# S9875 Rucaparib Selleckchem Cat# S4948 Niraparib (MK-4827) Selleckchem Cat# S2741 Veliparib Selleckchem Cat# S1004 Pamiparib Selleckchem Cat# S8592 E7449 (Stenoparib) Selleckchem Cat# S8419 A-966492 Selleckchem Cat# S2197 Olaparib (AZD2281) Selleckchem Cat# S1060 Experimental models: Cell lines Human: HeLa Kyoto ATCC CRL-11268; RRID:CVCL_1922 Human: HeLa Kyoto RFC4-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto PARP1-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto POLD2-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto POLH-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto RPA1-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto ADPRHL2-LAP cells The Hyman Laboratory, MPI-CBG 8494 Human: DLD1 Cell line Horizon Discovery Cat# HD 105-027; RRID:CVCL_0248 Human: DLD1 PARP1-LAP This paper N/A Human: PC3 Cell line RRID:CVCL_0035 Human: PC3 PARP1-LAP This paper N/A Software and algorithms CellTool Danovski et al.40 https://dnarepair.bas.bg/software/CellTool/

    Techniques:

    Figure 4. Kinetics of ARH3 at DNA damage sites upon PARPi (A–G) Kinetics of recruitment and removal of ARH3 at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the maximum total fluorescence intensity of ARH3 at DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PIC values calculated based on the mean maximum fluorescence intensity of ARH3 at DNA damage sites. (I) PARP1 residual activities and in vivo IC50 values. Error bars represent the SD. NT, no treatment; CI, confidence interval; n.d., not determined. See also Fig- ure S4.

    Journal: Cell reports

    Article Title: A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells.

    doi: 10.1016/j.celrep.2024.114234

    Figure Lengend Snippet: Figure 4. Kinetics of ARH3 at DNA damage sites upon PARPi (A–G) Kinetics of recruitment and removal of ARH3 at IR-induced DNA damage sites following treatment with (A) pamiparib, (B) veliparib, (C) olaparib, (D) rucaparib, (E) E7449, (F) niraparib, or (G) talazoparib. Boxplots depict the maximum total fluorescence intensity of ARH3 at DNA damage sites estimated via CRC modeling. Red dots indicate the mean value. (H) PIC values calculated based on the mean maximum fluorescence intensity of ARH3 at DNA damage sites. (I) PARP1 residual activities and in vivo IC50 values. Error bars represent the SD. NT, no treatment; CI, confidence interval; n.d., not determined. See also Fig- ure S4.

    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Chemicals, peptides, and recombinant proteins FluoroBrite DMEM Thermo Fisher Scientific Cat# A1896701 GlutaMAX Supplement Thermo Fisher Scientific Cat# 35050061 BMN673 (Talazoparib) Selleckchem Cat# S7048 AZD5305 (Saruparib) Selleckchem Cat# S9875 Rucaparib Selleckchem Cat# S4948 Niraparib (MK-4827) Selleckchem Cat# S2741 Veliparib Selleckchem Cat# S1004 Pamiparib Selleckchem Cat# S8592 E7449 (Stenoparib) Selleckchem Cat# S8419 A-966492 Selleckchem Cat# S2197 Olaparib (AZD2281) Selleckchem Cat# S1060 Experimental models: Cell lines Human: HeLa Kyoto ATCC CRL-11268; RRID:CVCL_1922 Human: HeLa Kyoto RFC4-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto PARP1-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto POLD2-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto POLH-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto RPA1-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto ADPRHL2-LAP cells The Hyman Laboratory, MPI-CBG 8494 Human: DLD1 Cell line Horizon Discovery Cat# HD 105-027; RRID:CVCL_0248 Human: DLD1 PARP1-LAP This paper N/A Human: PC3 Cell line RRID:CVCL_0035 Human: PC3 PARP1-LAP This paper N/A Software and algorithms CellTool Danovski et al.40 https://dnarepair.bas.bg/software/CellTool/

    Techniques: In Vivo

    Figure 6. PARPis rearrange downstream DNA repair events (A) Correlations between the average half-times of recruitment of RFC4, PCNA, POLD2, and POLH following PARPi and PRC values for evaluated PARPis. Error bars represent the SD. (B) Correlation between the extent of uncoupling of PCNA removal and RPA1 recruitment and PRC values for evaluated PARPis. The uncoupling is calculated as the average difference between the half-times of removal of PCNA and the half-times of recruitment of RPA1 at the single-cell level. Ruca- and niraparib have been removed from the correlation graph on the right as outliers. Error bars represent the SD. (C) Clonogenic assay of HeLa Kyoto cells treated with the indicated PARPi concentrations. (D) Mean surviving fractions ± SEM of HeLa Kyoto cells treated with the indicated PARPi concentrations (n = 3). (E) Cell viability IC50 values (half-maximal suppression of cell viability). Error bars represent the SEM. White dots indicate the mean value. P, pamiparib; V, ve- liparib; O, olaparib; R, rucaparib; E, E7449; N, niraparib; T, talazoparib; n.d., not determined. See also Figure S7.

    Journal: Cell reports

    Article Title: A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells.

    doi: 10.1016/j.celrep.2024.114234

    Figure Lengend Snippet: Figure 6. PARPis rearrange downstream DNA repair events (A) Correlations between the average half-times of recruitment of RFC4, PCNA, POLD2, and POLH following PARPi and PRC values for evaluated PARPis. Error bars represent the SD. (B) Correlation between the extent of uncoupling of PCNA removal and RPA1 recruitment and PRC values for evaluated PARPis. The uncoupling is calculated as the average difference between the half-times of removal of PCNA and the half-times of recruitment of RPA1 at the single-cell level. Ruca- and niraparib have been removed from the correlation graph on the right as outliers. Error bars represent the SD. (C) Clonogenic assay of HeLa Kyoto cells treated with the indicated PARPi concentrations. (D) Mean surviving fractions ± SEM of HeLa Kyoto cells treated with the indicated PARPi concentrations (n = 3). (E) Cell viability IC50 values (half-maximal suppression of cell viability). Error bars represent the SEM. White dots indicate the mean value. P, pamiparib; V, ve- liparib; O, olaparib; R, rucaparib; E, E7449; N, niraparib; T, talazoparib; n.d., not determined. See also Figure S7.

    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Chemicals, peptides, and recombinant proteins FluoroBrite DMEM Thermo Fisher Scientific Cat# A1896701 GlutaMAX Supplement Thermo Fisher Scientific Cat# 35050061 BMN673 (Talazoparib) Selleckchem Cat# S7048 AZD5305 (Saruparib) Selleckchem Cat# S9875 Rucaparib Selleckchem Cat# S4948 Niraparib (MK-4827) Selleckchem Cat# S2741 Veliparib Selleckchem Cat# S1004 Pamiparib Selleckchem Cat# S8592 E7449 (Stenoparib) Selleckchem Cat# S8419 A-966492 Selleckchem Cat# S2197 Olaparib (AZD2281) Selleckchem Cat# S1060 Experimental models: Cell lines Human: HeLa Kyoto ATCC CRL-11268; RRID:CVCL_1922 Human: HeLa Kyoto RFC4-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto PARP1-LAP/mPCNA-mCherry cells This paper N/A Human: HeLa Kyoto POLD2-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto POLH-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto RPA1-LAP/mPCNA-mCherry cells Aleksandrov et al.5 N/A Human: HeLa Kyoto ADPRHL2-LAP cells The Hyman Laboratory, MPI-CBG 8494 Human: DLD1 Cell line Horizon Discovery Cat# HD 105-027; RRID:CVCL_0248 Human: DLD1 PARP1-LAP This paper N/A Human: PC3 Cell line RRID:CVCL_0035 Human: PC3 PARP1-LAP This paper N/A Software and algorithms CellTool Danovski et al.40 https://dnarepair.bas.bg/software/CellTool/

    Techniques: Clonogenic Assay

    Melphalan reduces viability and induces apoptosis of HPV16 positive tonsillar cancer cells. ( a ) MTT assay on HN26 cells incubated for 24 h with 100 μM of the indicated cancer drugs or carrier substance DMSO. Mean values of triplicates are shown. ( b ) Viability of C33A2 cervical cancer cells, HN7 head and neck cancer cells or HN26 tonsillar cancer cells treated with DMSO or 100 μM melphalan for the indicated time periods was determined with an MTT assay as described in Materials and Methods and plotted against time in melphalan. ( c – e ) Western blots of full length and cleaved poly [ADP‐ribose] polymerase (PARP1) in extracts from HN26 cells, HN7 cells or1 C33A2 cells treated with 100 μM melphalan for the indicated time periods. Poly ADP‐ribosylation (parylation) was monitored by Western blotting with monospecific antibody to poly (ADP‐ribose) (PAR) in cell extracts from HN26 cells ( f ) or C33A2 cells ( h ) treated with 100 μM melphalan for the indicated time periods. ( g ) Western blotting with monospecific antibody to poly (ADP‐ribose) (PAR) in HN26 cells treated with 100 μM melphalan in the absence or presence of PARP1 inhibitor A‐966492. ( i ) Apoptosis‐mediated release of mitochondrial cytochrome c into the cytoplasmic space as a marker for apoptosis in HN26 cells treated with 100 μM melphalan for the indicated time points. Method is described in Supporting Information methods. Antibody is listed in Supporting Information Table . D, DMSO.

    Journal: International Journal of Cancer

    Article Title: Short half‐life of HPV16 E6 and E7 mRNAs sensitizes HPV16‐positive tonsillar cancer cell line HN26 to DNA‐damaging drugs

    doi: 10.1002/ijc.31918

    Figure Lengend Snippet: Melphalan reduces viability and induces apoptosis of HPV16 positive tonsillar cancer cells. ( a ) MTT assay on HN26 cells incubated for 24 h with 100 μM of the indicated cancer drugs or carrier substance DMSO. Mean values of triplicates are shown. ( b ) Viability of C33A2 cervical cancer cells, HN7 head and neck cancer cells or HN26 tonsillar cancer cells treated with DMSO or 100 μM melphalan for the indicated time periods was determined with an MTT assay as described in Materials and Methods and plotted against time in melphalan. ( c – e ) Western blots of full length and cleaved poly [ADP‐ribose] polymerase (PARP1) in extracts from HN26 cells, HN7 cells or1 C33A2 cells treated with 100 μM melphalan for the indicated time periods. Poly ADP‐ribosylation (parylation) was monitored by Western blotting with monospecific antibody to poly (ADP‐ribose) (PAR) in cell extracts from HN26 cells ( f ) or C33A2 cells ( h ) treated with 100 μM melphalan for the indicated time periods. ( g ) Western blotting with monospecific antibody to poly (ADP‐ribose) (PAR) in HN26 cells treated with 100 μM melphalan in the absence or presence of PARP1 inhibitor A‐966492. ( i ) Apoptosis‐mediated release of mitochondrial cytochrome c into the cytoplasmic space as a marker for apoptosis in HN26 cells treated with 100 μM melphalan for the indicated time points. Method is described in Supporting Information methods. Antibody is listed in Supporting Information Table . D, DMSO.

    Article Snippet: The after substances were purchased: Melphalan hydrochloride (Y0001158, Sigma), Etiposide (S1225, Selleckchem), Cisplatin (S1166, Selleckchem), actinomycin D (A9415, Sigma), alpha‐amanitin (A2263, Sigma) and PARP1 inhibitor A‐966492 (S2197, Selleckchem).

    Techniques: MTT Assay, Incubation, Western Blot, Marker

    Melphalan activates p53 in HPV16 positive tonsillar cancer cells. ( a ) Western blot with monospecific antibody to p53 or actin on extracts from HN26 or 293T cells. Extract from 293T cells serves as a positive control for p53 protein. ( b ) Western blot with monospecific antibody to p53 or actin on extracts from C33A2 cells treated with DMSO or 100 μM melphalan for the indicated time points. ( c , d ) Western blot with monospecific antibody to p53 or actin on extracts from HN26 cells treated with DMSO or melphalan for the indicated time points. Two different concentrations of melphalan were used in c (100 μM) and d (50 μM). ( e ) Western blot with monospecific antibody to PARP1, caspase 3, p53 or actin on extracts from HPV16‐immortalized human keratinocyte cell line 3,310 treated with DMSO or 100 μM melphalan for the indicated time points. ( f ) Western blots with monospecific antibodies to phosphorylated ATM (p‐ATM), ATM, phosphorylated Chk1 (p‐Chk1), Chk1 or actin on extracts from 3,310 cells treated with DMSO or 100 μM melphalan for the indicated time points.

    Journal: International Journal of Cancer

    Article Title: Short half‐life of HPV16 E6 and E7 mRNAs sensitizes HPV16‐positive tonsillar cancer cell line HN26 to DNA‐damaging drugs

    doi: 10.1002/ijc.31918

    Figure Lengend Snippet: Melphalan activates p53 in HPV16 positive tonsillar cancer cells. ( a ) Western blot with monospecific antibody to p53 or actin on extracts from HN26 or 293T cells. Extract from 293T cells serves as a positive control for p53 protein. ( b ) Western blot with monospecific antibody to p53 or actin on extracts from C33A2 cells treated with DMSO or 100 μM melphalan for the indicated time points. ( c , d ) Western blot with monospecific antibody to p53 or actin on extracts from HN26 cells treated with DMSO or melphalan for the indicated time points. Two different concentrations of melphalan were used in c (100 μM) and d (50 μM). ( e ) Western blot with monospecific antibody to PARP1, caspase 3, p53 or actin on extracts from HPV16‐immortalized human keratinocyte cell line 3,310 treated with DMSO or 100 μM melphalan for the indicated time points. ( f ) Western blots with monospecific antibodies to phosphorylated ATM (p‐ATM), ATM, phosphorylated Chk1 (p‐Chk1), Chk1 or actin on extracts from 3,310 cells treated with DMSO or 100 μM melphalan for the indicated time points.

    Article Snippet: The after substances were purchased: Melphalan hydrochloride (Y0001158, Sigma), Etiposide (S1225, Selleckchem), Cisplatin (S1166, Selleckchem), actinomycin D (A9415, Sigma), alpha‐amanitin (A2263, Sigma) and PARP1 inhibitor A‐966492 (S2197, Selleckchem).

    Techniques: Western Blot, Positive Control

    Actinomycin D causes rapid degradation of HPV16 E6 and E7 oncogene mRNAs in HPV16 positive tonsillar cancer cells. ( a ) RT‐PCR on total RNA extracted from HN26 cells treated with DMSO alone or 1.5 μM of actinomycin D for the indicated time periods. HPV16 E4, E6, E6*I/E7 and E6*II/E7 mRNAs were monitored as well as spliced cellular gapdh mRNA. The location of the RT‐PCR primers in the HPV16 genome is shown in Supporting Information Figure 5B. ( b ) The RT‐PCR bands representing HPV16 mRNAs were quantified and plotted against hours of 1.5 μM actinomycin D treatment of the HN26 cells. ( c ) Western blot with monospecific antibody to p53 on extracts from 293T cells or HN26 cells treated with DMSO (D) or actinomycin D for the indicated time points. ( d ) Western blot with monospecific antibody to PARP1 on extracts from HN26 cells treated with DMSO (D) or 1.5 μM actinomycin D for the indicated time points. ( e ) RT‐PCR on total RNA extracted from HN26 cells treated with DMSO alone or 3 μg/mL of alpha‐amanitin for the indicated time periods. HPV16 E6, E6*I/E7 and E6*II/E7 mRNAs were monitored as well as spliced cellular gapdh mRNA. ( f ) Western blot on extracts from HN26 cells incubated with DMSO (D) or 3 μg/mL of alpha‐amanitin for 9 h with monospecific antibody to RNA polymerase II and actin. ( g ) Western blot with monospecific antibody to PARP1 on extracts from HN26 cells treated with DMSO (D) or 3 μg/mL alpha‐amanitin for the indicated time points. (H) Western blot with monospecific antibody to p53 on extracts from 293T cells or HN26 cells treated with DMSO (D) or alpha‐amanitin (3 μg/mL) for the indicated time points.

    Journal: International Journal of Cancer

    Article Title: Short half‐life of HPV16 E6 and E7 mRNAs sensitizes HPV16‐positive tonsillar cancer cell line HN26 to DNA‐damaging drugs

    doi: 10.1002/ijc.31918

    Figure Lengend Snippet: Actinomycin D causes rapid degradation of HPV16 E6 and E7 oncogene mRNAs in HPV16 positive tonsillar cancer cells. ( a ) RT‐PCR on total RNA extracted from HN26 cells treated with DMSO alone or 1.5 μM of actinomycin D for the indicated time periods. HPV16 E4, E6, E6*I/E7 and E6*II/E7 mRNAs were monitored as well as spliced cellular gapdh mRNA. The location of the RT‐PCR primers in the HPV16 genome is shown in Supporting Information Figure 5B. ( b ) The RT‐PCR bands representing HPV16 mRNAs were quantified and plotted against hours of 1.5 μM actinomycin D treatment of the HN26 cells. ( c ) Western blot with monospecific antibody to p53 on extracts from 293T cells or HN26 cells treated with DMSO (D) or actinomycin D for the indicated time points. ( d ) Western blot with monospecific antibody to PARP1 on extracts from HN26 cells treated with DMSO (D) or 1.5 μM actinomycin D for the indicated time points. ( e ) RT‐PCR on total RNA extracted from HN26 cells treated with DMSO alone or 3 μg/mL of alpha‐amanitin for the indicated time periods. HPV16 E6, E6*I/E7 and E6*II/E7 mRNAs were monitored as well as spliced cellular gapdh mRNA. ( f ) Western blot on extracts from HN26 cells incubated with DMSO (D) or 3 μg/mL of alpha‐amanitin for 9 h with monospecific antibody to RNA polymerase II and actin. ( g ) Western blot with monospecific antibody to PARP1 on extracts from HN26 cells treated with DMSO (D) or 3 μg/mL alpha‐amanitin for the indicated time points. (H) Western blot with monospecific antibody to p53 on extracts from 293T cells or HN26 cells treated with DMSO (D) or alpha‐amanitin (3 μg/mL) for the indicated time points.

    Article Snippet: The after substances were purchased: Melphalan hydrochloride (Y0001158, Sigma), Etiposide (S1225, Selleckchem), Cisplatin (S1166, Selleckchem), actinomycin D (A9415, Sigma), alpha‐amanitin (A2263, Sigma) and PARP1 inhibitor A‐966492 (S2197, Selleckchem).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Incubation