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p21 c 19  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology p21 c 19
    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; <t>p21,</t> cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.
    P21 C 19, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 5570 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c+19/pmc12945421-34-94-97?v=Santa+Cruz+Biotechnology
    Average 96 stars, based on 5570 article reviews
    p21 c 19 - by Bioz Stars, 2026-07
    96/100 stars

    Images

    1) Product Images from "Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity"

    Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

    Journal: International Journal of Oncology

    doi: 10.3892/ijo.2026.5861

    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; p21, cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.
    Figure Legend Snippet: Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; p21, cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.

    Techniques Used: Activation Assay, Staining, Control, Expressing, Western Blot

    Influence of combined treatment of A2780ADR cells with Doxo and selected inhibitors on mechanism of the DDR and mRNA expression of selected susceptibility-related genes. (A) Logarithmically growing A2780ADR cells were co-treated with the indicated concentrations of Doxo and selected pharmacological inhibitors (concentrations see ) for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting. For loading control, blots were reprobed with ERK2 antibody. (B) Reverse transcription-quantitative PCR of the mRNA expression of selected factors known to contribute to different mechanisms of drug sensitivity. Data shown are mean ± SD from triplicate determinations as described in methods. Relative mRNA level in untreated A2780ADR cells was set to 1.0. Doxo, doxorubicin; DDR, DNA damage response; p-, phosphorylated; nd, not detectable; Bax, Bcl-2 associated protein X; Bcl-2, B-cell lymphoma; BBC3, Bcl-2 binding component 2; BRCA1, 2, breast cancer associated gene 1,2; Cl casp-7, cleaved caspase 7; Chk, checkpoint kinase; CXCL8, chemokine ligand 8 (interleukin 8); p21, CDK inhibitor 1; p16, CDK inhibitor 2; CDKN1A/2A, cyclin dependent kinae inhibitor 1A/2A; CCNB1, Cyclin B1; b-Gal, beta-galactosidase; FASL, FAS ligand; FASR, FAS receptor; GADD, growth arrest and DNA damage inducible GPX1, glutathione peroxidase 1; GSTM1, glutathione S-transferase 1; HMOX1, heme oxygenase 1; γH2AX, Ser139 phosphorylated histone H2AX; p53, tumor suppressor p53; PARP, poly (ADP-ribose) polymerase; PCNA-proliferating cell nuclear antigen; PGC1A, PPARG coactivator 1; PPARGC1A, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; RAD51, radiation damage gene 51; RPAreplication protein A; SOD1, superoxide dismutase 1; Ver, verapamil.
    Figure Legend Snippet: Influence of combined treatment of A2780ADR cells with Doxo and selected inhibitors on mechanism of the DDR and mRNA expression of selected susceptibility-related genes. (A) Logarithmically growing A2780ADR cells were co-treated with the indicated concentrations of Doxo and selected pharmacological inhibitors (concentrations see ) for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting. For loading control, blots were reprobed with ERK2 antibody. (B) Reverse transcription-quantitative PCR of the mRNA expression of selected factors known to contribute to different mechanisms of drug sensitivity. Data shown are mean ± SD from triplicate determinations as described in methods. Relative mRNA level in untreated A2780ADR cells was set to 1.0. Doxo, doxorubicin; DDR, DNA damage response; p-, phosphorylated; nd, not detectable; Bax, Bcl-2 associated protein X; Bcl-2, B-cell lymphoma; BBC3, Bcl-2 binding component 2; BRCA1, 2, breast cancer associated gene 1,2; Cl casp-7, cleaved caspase 7; Chk, checkpoint kinase; CXCL8, chemokine ligand 8 (interleukin 8); p21, CDK inhibitor 1; p16, CDK inhibitor 2; CDKN1A/2A, cyclin dependent kinae inhibitor 1A/2A; CCNB1, Cyclin B1; b-Gal, beta-galactosidase; FASL, FAS ligand; FASR, FAS receptor; GADD, growth arrest and DNA damage inducible GPX1, glutathione peroxidase 1; GSTM1, glutathione S-transferase 1; HMOX1, heme oxygenase 1; γH2AX, Ser139 phosphorylated histone H2AX; p53, tumor suppressor p53; PARP, poly (ADP-ribose) polymerase; PCNA-proliferating cell nuclear antigen; PGC1A, PPARG coactivator 1; PPARGC1A, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; RAD51, radiation damage gene 51; RPAreplication protein A; SOD1, superoxide dismutase 1; Ver, verapamil.

    Techniques Used: Expressing, Western Blot, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Binding Assay



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    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; <t>p21,</t> cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.
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    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; <t>p21,</t> cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.
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    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; <t>p21,</t> cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.
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    Image Search Results


    Simplified ‘non-hydroxylation’ gibberellin pathway in Arabidopsis. Enzymes are labelled in grey; CPS, ent -copalyl pyrophosphate synthase; KS, ent -kaurene synthase; KO, ent -kaurene oxidase; KAO, ent -kaurenoic acid oxidase; 20ox, gibberellin 20-oxidase; 3ox, gibberellin 3-oxidase; 2ox, gibberellin 2-oxidase. Central precursor GA 12 and bioactive GA 4 are highlighted in bold characters.

    Journal: bioRxiv

    Article Title: A single UV-C pulse modulates Gibberellin homeostasis and Plant Development in Arabidopsis

    doi: 10.64898/2026.04.28.721437

    Figure Lengend Snippet: Simplified ‘non-hydroxylation’ gibberellin pathway in Arabidopsis. Enzymes are labelled in grey; CPS, ent -copalyl pyrophosphate synthase; KS, ent -kaurene synthase; KO, ent -kaurene oxidase; KAO, ent -kaurenoic acid oxidase; 20ox, gibberellin 20-oxidase; 3ox, gibberellin 3-oxidase; 2ox, gibberellin 2-oxidase. Central precursor GA 12 and bioactive GA 4 are highlighted in bold characters.

    Article Snippet: The C 19 -2ox quintuple mutant ( 2ox1, 2ox2, 2ox3, 2ox4, 2ox6 ) is in the Col-0 background and was a gift from Dr. Andy Philipps (Rothamsted Research, UK).

    Techniques:

    Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; p21, cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.

    Journal: International Journal of Oncology

    Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

    doi: 10.3892/ijo.2026.5861

    Figure Lengend Snippet: Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; p21, cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.

    Article Snippet: The following primary antibodies were used: Copper transporting ATPase (ATP7A), extracellular regulated kinase 2 (ERK2), phosphorylated (p)-histone H3 (Ser10) from Thermo Fisher Scientific Inc., cleaved caspase-7 (Asp198), p-Chk1 (Ser 345), cyclin B1, galactosidase β (E2U2I), GAPDH (14C10), MDR1/ABCB1 (D3H1Q), p-P53 (S15), PARP, TopBP1(D8G4L), topoisomerase IIa (D10G9), 53BP1 and Ki67 were from Cell Signaling Technology Inc., pChk2 (T68) [Y171], copper uptake protein 1 (CTR1/SLC31A1) [EPR7936] and Rad51 from Abcam, γH2AX (Ser 139) clone JBW301, p-KAP-1 (S824) and p-RPA32 (S4/S8) from Bethyl Laboratories Inc., organic cation transporter-2 (OCT2) from Biozol Diagnostics Vertrieb GmbH, p16 (F-12) and p21 (C-19) from Santa Cruz Biotechnology, Inc. As secondary antibodies, horseradish peroxidase-conjugated secondary antibodies goat anti-mouse IgG and mouse anti-rabbit IgG were used (Rockland Immunochemicals Inc.).

    Techniques: Activation Assay, Staining, Control, Expressing, Western Blot

    Influence of combined treatment of A2780ADR cells with Doxo and selected inhibitors on mechanism of the DDR and mRNA expression of selected susceptibility-related genes. (A) Logarithmically growing A2780ADR cells were co-treated with the indicated concentrations of Doxo and selected pharmacological inhibitors (concentrations see ) for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting. For loading control, blots were reprobed with ERK2 antibody. (B) Reverse transcription-quantitative PCR of the mRNA expression of selected factors known to contribute to different mechanisms of drug sensitivity. Data shown are mean ± SD from triplicate determinations as described in methods. Relative mRNA level in untreated A2780ADR cells was set to 1.0. Doxo, doxorubicin; DDR, DNA damage response; p-, phosphorylated; nd, not detectable; Bax, Bcl-2 associated protein X; Bcl-2, B-cell lymphoma; BBC3, Bcl-2 binding component 2; BRCA1, 2, breast cancer associated gene 1,2; Cl casp-7, cleaved caspase 7; Chk, checkpoint kinase; CXCL8, chemokine ligand 8 (interleukin 8); p21, CDK inhibitor 1; p16, CDK inhibitor 2; CDKN1A/2A, cyclin dependent kinae inhibitor 1A/2A; CCNB1, Cyclin B1; b-Gal, beta-galactosidase; FASL, FAS ligand; FASR, FAS receptor; GADD, growth arrest and DNA damage inducible GPX1, glutathione peroxidase 1; GSTM1, glutathione S-transferase 1; HMOX1, heme oxygenase 1; γH2AX, Ser139 phosphorylated histone H2AX; p53, tumor suppressor p53; PARP, poly (ADP-ribose) polymerase; PCNA-proliferating cell nuclear antigen; PGC1A, PPARG coactivator 1; PPARGC1A, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; RAD51, radiation damage gene 51; RPAreplication protein A; SOD1, superoxide dismutase 1; Ver, verapamil.

    Journal: International Journal of Oncology

    Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

    doi: 10.3892/ijo.2026.5861

    Figure Lengend Snippet: Influence of combined treatment of A2780ADR cells with Doxo and selected inhibitors on mechanism of the DDR and mRNA expression of selected susceptibility-related genes. (A) Logarithmically growing A2780ADR cells were co-treated with the indicated concentrations of Doxo and selected pharmacological inhibitors (concentrations see ) for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting. For loading control, blots were reprobed with ERK2 antibody. (B) Reverse transcription-quantitative PCR of the mRNA expression of selected factors known to contribute to different mechanisms of drug sensitivity. Data shown are mean ± SD from triplicate determinations as described in methods. Relative mRNA level in untreated A2780ADR cells was set to 1.0. Doxo, doxorubicin; DDR, DNA damage response; p-, phosphorylated; nd, not detectable; Bax, Bcl-2 associated protein X; Bcl-2, B-cell lymphoma; BBC3, Bcl-2 binding component 2; BRCA1, 2, breast cancer associated gene 1,2; Cl casp-7, cleaved caspase 7; Chk, checkpoint kinase; CXCL8, chemokine ligand 8 (interleukin 8); p21, CDK inhibitor 1; p16, CDK inhibitor 2; CDKN1A/2A, cyclin dependent kinae inhibitor 1A/2A; CCNB1, Cyclin B1; b-Gal, beta-galactosidase; FASL, FAS ligand; FASR, FAS receptor; GADD, growth arrest and DNA damage inducible GPX1, glutathione peroxidase 1; GSTM1, glutathione S-transferase 1; HMOX1, heme oxygenase 1; γH2AX, Ser139 phosphorylated histone H2AX; p53, tumor suppressor p53; PARP, poly (ADP-ribose) polymerase; PCNA-proliferating cell nuclear antigen; PGC1A, PPARG coactivator 1; PPARGC1A, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; RAD51, radiation damage gene 51; RPAreplication protein A; SOD1, superoxide dismutase 1; Ver, verapamil.

    Article Snippet: The following primary antibodies were used: Copper transporting ATPase (ATP7A), extracellular regulated kinase 2 (ERK2), phosphorylated (p)-histone H3 (Ser10) from Thermo Fisher Scientific Inc., cleaved caspase-7 (Asp198), p-Chk1 (Ser 345), cyclin B1, galactosidase β (E2U2I), GAPDH (14C10), MDR1/ABCB1 (D3H1Q), p-P53 (S15), PARP, TopBP1(D8G4L), topoisomerase IIa (D10G9), 53BP1 and Ki67 were from Cell Signaling Technology Inc., pChk2 (T68) [Y171], copper uptake protein 1 (CTR1/SLC31A1) [EPR7936] and Rad51 from Abcam, γH2AX (Ser 139) clone JBW301, p-KAP-1 (S824) and p-RPA32 (S4/S8) from Bethyl Laboratories Inc., organic cation transporter-2 (OCT2) from Biozol Diagnostics Vertrieb GmbH, p16 (F-12) and p21 (C-19) from Santa Cruz Biotechnology, Inc. As secondary antibodies, horseradish peroxidase-conjugated secondary antibodies goat anti-mouse IgG and mouse anti-rabbit IgG were used (Rockland Immunochemicals Inc.).

    Techniques: Expressing, Western Blot, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Binding Assay