rabbit anti dna binding protein 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti dna binding protein 2
    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; <t>DDB2,</t> DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Rabbit Anti Dna Binding Protein 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti dna binding protein 2/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti dna binding protein 2 - by Bioz Stars, 2023-03
    92/100 stars

    Images

    1) Product Images from "Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells"

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00160.2018

    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Techniques Used: Immunolabeling, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Binding Assay

    p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Techniques Used: Western Blot, Binding Assay, Knock-Out, Immunolabeling, Staining

    rabbit anti dna binding protein 2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc rabbit anti dna binding protein 2
    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; <t>DDB2,</t> DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Rabbit Anti Dna Binding Protein 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti dna binding protein 2/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti dna binding protein 2 - by Bioz Stars, 2023-03
    92/100 stars

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    1) Product Images from "Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells"

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00160.2018

    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Techniques Used: Immunolabeling, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Binding Assay

    p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Techniques Used: Western Blot, Binding Assay, Knock-Out, Immunolabeling, Staining

    rabbit anti dna binding protein 2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Structured Review

    Cell Signaling Technology Inc rabbit anti dna binding protein 2
    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; <t>DDB2,</t> DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Rabbit Anti Dna Binding Protein 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti dna binding protein 2/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti dna binding protein 2 - by Bioz Stars, 2023-03
    94/100 stars

    Images

    1) Product Images from "Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells"

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00160.2018

    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Techniques Used: Immunolabeling, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Binding Assay

    p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Techniques Used: Western Blot, Binding Assay, Knock-Out, Immunolabeling, Staining

    rabbit anti dna binding protein 2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Structured Review

    Cell Signaling Technology Inc rabbit anti dna binding protein 2
    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; <t>DDB2,</t> DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Rabbit Anti Dna Binding Protein 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti dna binding protein 2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti dna binding protein 2 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells"

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.00160.2018

    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Techniques Used: Immunolabeling, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Binding Assay

    p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.
    Figure Legend Snippet: p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Techniques Used: Western Blot, Binding Assay, Knock-Out, Immunolabeling, Staining

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    Cell Signaling Technology Inc rabbit anti dna binding protein 2
    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; <t>DDB2,</t> DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.
    Rabbit Anti Dna Binding Protein 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    doi: 10.1152/ajpheart.00160.2018

    Figure Lengend Snippet: p53 transactivation domain (TAD) deletion does not affect pluripotent markers in human induced pluripotent stem cells (hiPSCs). A: representative images of Oct4-, Sox2-, and Nanog-immunolabeled (red) p53-TAD knockout (KO) hiPSCs. Phalloidin is shown in green; the nucleus is shown in blue. B−D: mRNA transcript levels of pluripotent markers (B), p53-regulated genes (C), and p53-regulated DNA repair genes (D) in wild-type (WT) and p53-TAD KO hiPSCs as measured by RT-PCR. Symbols denote plotted values. Data are means ± SD; n = 3. *P < 0.05 vs. WT. RQ, relative quantity; a.u., arbitrary units; CDKN1A, cyclin-dependent kinase inhibitor 1A; PIDD, p53-induced death domain; XPA, xeroderma pigmentosum group A; DDB2, DNA-binding protein 2; IGF1R, insulin-like growth factor 1 receptor; DNA Pol η, DNA polymerase H; XPD, xeroderma pigmentosum group D; BBC3, Bcl-2-binding component 3.

    Article Snippet: The following antibodies were used: NH 2 -terminal-specific rabbit monoclonal anti-p53 (Cell Signaling Technology, Danvers, MA), rabbit COOH-terminal anti-p53 (Sigma-Aldrich), rabbit monoclonal anti-checkpoint kinase 2 (Chk2; Thr 68 , Cell Signaling Technology), rabbit monoclonal anti-Chk2 (Cell Signaling Technology), rabbit monoclonal anti-Mre11 (Cell Signaling Technology), rabbit anti-Rad50 (Cell Signaling Technology), rabbit anti-xeroderma pigmentosum group D (XPD; D3Z6I, Cell Signaling Technology), rabbit anti-xeroderma pigmentosum group A (XPA; D9U5U, Cell Signaling Technology), rabbit anti-DNA polymerase H (DNA Pol η; E1I7T, Cell Signaling Technology), and rabbit anti-DNA-binding protein 2 (DDB2; D4C4, Cell Signaling Technology).

    Techniques: Immunolabeling, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Binding Assay

    p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    Article Title: Transactivation domain of p53 regulates DNA repair and integrity in human iPS cells

    doi: 10.1152/ajpheart.00160.2018

    Figure Lengend Snippet: p53 transactivation domain (TAD) deletion impairs DNA damage repair in human induced pluripotent stem cells (hiPSCs). A and B, left: Western blots of Rad50, Mre11, phosphorylated checkpoint kinase 2 (p-Chk2) at Thr68, and total Chk2 (A) as well as xeroderma pigmentosum group D (XPD), xeroderma pigmentosum group A (XPA), DNA-binding protein 2 (DDB2), and DNA polymerase H (DNA Pol η) (B) in wild-type (WT) and p53-TAD knockout (KO) hiPSCs with and without doxorubicin (Doxo) treatment. Western blot quantifications are shown on the right. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. the respective nontreated cells; †P < 0.05 vs. WT; ‡P < 0.05 vs. WT + Doxo. C: p53-TAD hiPSCs were immunolabeled for γH2A.X (green; left) and counterstained with DAPI (blue; right). D: schematic of DNA damage repair methodology. E: nucleoids in WT hiPSCs and p53-TAD KO hiPSCs treated with Doxo (top) and after recovery (bottom) were stained with Vista green dye (green). Comets were apparent with Doxo and after recovery of p53-TAD KO hiPSCs, whereas intact DNA was noted in WT hiPSCs after recovery. F: tail moment of WT hiPSCs and p53-TAD KO hiPSCs nuclei at baseline (control), after Doxo, and after recovery. a.u., arbitrary units. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. control; **P < 0.05 vs. Doxo. G: representative micrograph of hiPSCs immunolabeled for γH2A.X (green; left) and nuclei stained with DAPI (blue; right). H: fraction of WT p53 and p53-TAD KO hiPSCs positive for γH2A.X. Symbols denote plotted values. Data are means ± SD; n = 3 in all cases. *P < 0.05 vs. WT.

    Article Snippet: The following antibodies were used: NH 2 -terminal-specific rabbit monoclonal anti-p53 (Cell Signaling Technology, Danvers, MA), rabbit COOH-terminal anti-p53 (Sigma-Aldrich), rabbit monoclonal anti-checkpoint kinase 2 (Chk2; Thr 68 , Cell Signaling Technology), rabbit monoclonal anti-Chk2 (Cell Signaling Technology), rabbit monoclonal anti-Mre11 (Cell Signaling Technology), rabbit anti-Rad50 (Cell Signaling Technology), rabbit anti-xeroderma pigmentosum group D (XPD; D3Z6I, Cell Signaling Technology), rabbit anti-xeroderma pigmentosum group A (XPA; D9U5U, Cell Signaling Technology), rabbit anti-DNA polymerase H (DNA Pol η; E1I7T, Cell Signaling Technology), and rabbit anti-DNA-binding protein 2 (DDB2; D4C4, Cell Signaling Technology).

    Techniques: Western Blot, Binding Assay, Knock-Out, Immunolabeling, Staining