p53 1c12 mouse mab Cell Signaling Technology Inc Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 90
    Cell Signaling Technology Inc p53
    Effect of ATM or <t>p53</t> inhibition on DNA damage repair and hair cell survival 3D images of OHC nuclei taken from the basal regions of organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification analysis of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA followed by post hoc Tukey's test (*** P ≤ 0.0004; CDDP versus control, or CDDP versus CDDP + KU55933). Confocal images showing the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the numbers of surviving IHCs (red bars) and OHCs (blue bars) for all treatment conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.03, ** P = 0.004, *** P ≤ 0.0008; CDDP versus control, or CDDP versus CDDP + KU55933). 3D images of OHC nuclei from the basal regions of organ of Corti cultures treated with culture medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0007; CDDP versus control). Data information: All experiments were performed in triplicate.
    P53, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 6102 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p53/product/Cell Signaling Technology Inc
    Average 90 stars, based on 6102 article reviews
    Price from $9.99 to $1999.99
    p53 - by Bioz Stars, 2020-02
    90/100 stars
      Buy from Supplier

    90
    Cell Signaling Technology Inc anti p53 mouse monoclonal
    Effect of ATM or <t>p53</t> inhibition on DNA damage repair and hair cell survival 3D images of OHC nuclei taken from the basal regions of organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification analysis of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA followed by post hoc Tukey's test (*** P ≤ 0.0004; CDDP versus control, or CDDP versus CDDP + KU55933). Confocal images showing the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the numbers of surviving IHCs (red bars) and OHCs (blue bars) for all treatment conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.03, ** P = 0.004, *** P ≤ 0.0008; CDDP versus control, or CDDP versus CDDP + KU55933). 3D images of OHC nuclei from the basal regions of organ of Corti cultures treated with culture medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0007; CDDP versus control). Data information: All experiments were performed in triplicate.
    Anti P53 Mouse Monoclonal, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p53 mouse monoclonal/product/Cell Signaling Technology Inc
    Average 90 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    anti p53 mouse monoclonal - by Bioz Stars, 2020-02
    90/100 stars
      Buy from Supplier

    82
    Cell Signaling Technology Inc mouse monoclonal p53
    Analysis of <t>telethonin/p53</t> co-localization
    Mouse Monoclonal P53, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 82/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal p53/product/Cell Signaling Technology Inc
    Average 82 stars, based on 22 article reviews
    Price from $9.99 to $1999.99
    mouse monoclonal p53 - by Bioz Stars, 2020-02
    82/100 stars
      Buy from Supplier

    Image Search Results


    Effect of ATM or p53 inhibition on DNA damage repair and hair cell survival 3D images of OHC nuclei taken from the basal regions of organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification analysis of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA followed by post hoc Tukey's test (*** P ≤ 0.0004; CDDP versus control, or CDDP versus CDDP + KU55933). Confocal images showing the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the numbers of surviving IHCs (red bars) and OHCs (blue bars) for all treatment conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.03, ** P = 0.004, *** P ≤ 0.0008; CDDP versus control, or CDDP versus CDDP + KU55933). 3D images of OHC nuclei from the basal regions of organ of Corti cultures treated with culture medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0007; CDDP versus control). Data information: All experiments were performed in triplicate.

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: Effect of ATM or p53 inhibition on DNA damage repair and hair cell survival 3D images of OHC nuclei taken from the basal regions of organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification analysis of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA followed by post hoc Tukey's test (*** P ≤ 0.0004; CDDP versus control, or CDDP versus CDDP + KU55933). Confocal images showing the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the numbers of surviving IHCs (red bars) and OHCs (blue bars) for all treatment conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.03, ** P = 0.004, *** P ≤ 0.0008; CDDP versus control, or CDDP versus CDDP + KU55933). 3D images of OHC nuclei from the basal regions of organ of Corti cultures treated with culture medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 1 day and immunolabeled for 53BP1 (green) and Hoechst 33342 (blue). Scale bar = 5 μm. Quantification of 53BP1 foci number per nucleus in both IHCs (red bars) and OHCs (blue bars) for all conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0007; CDDP versus control). Data information: All experiments were performed in triplicate.

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Inhibition, Immunolabeling

    Activation of the ATM‐Chk2‐p53 pathway upon CDDP treatment Confocal images showing the basal region of organ of Corti cultures treated with either culture medium alone or medium containing 10 μM CDDP for 1 day and immunolabeled for myosin 7A (red) and p‐ATM (green). Scale bar = 15 μm. Higher magnification images showing representative OHC and IHC nuclei from control and CDDP‐exposed cells. Scale bar = 5 μm. Histograms displaying green fluorescent signal intensity of x ‐projections of OHC and IHC nuclei from control and CDDP‐exposed cells. Quantification analysis of p‐ATM foci numbers in both OHCs and IHCs exposed to either culture medium alone (light blue and red lines for OHCs and IHCs, respectively) or 10 μM CDDP (blue and red lines for OHCs and IHCs, respectively; n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: Activation of the ATM‐Chk2‐p53 pathway upon CDDP treatment Confocal images showing the basal region of organ of Corti cultures treated with either culture medium alone or medium containing 10 μM CDDP for 1 day and immunolabeled for myosin 7A (red) and p‐ATM (green). Scale bar = 15 μm. Higher magnification images showing representative OHC and IHC nuclei from control and CDDP‐exposed cells. Scale bar = 5 μm. Histograms displaying green fluorescent signal intensity of x ‐projections of OHC and IHC nuclei from control and CDDP‐exposed cells. Quantification analysis of p‐ATM foci numbers in both OHCs and IHCs exposed to either culture medium alone (light blue and red lines for OHCs and IHCs, respectively) or 10 μM CDDP (blue and red lines for OHCs and IHCs, respectively; n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Activation Assay, Immunolabeling, Immunohistochemistry

    Intratympanic injection, tumor histology, and p53 genotyping and activation in vivo Shown is the custom‐made microendoscope. It consists of a fiber optic lens (10,000‐pixel resolution) for viewing and one catheter channel equipped with a fine needle for drug delivery. The blue arrowhead indicates the needle. Endoscopic view of the tympanic membrane (left image) and intratympanic injection through a fine needle (right image). The blue arrowhead indicates the needle. Representative scanned images of hematoxylin–eosin–safranin‐stained TP53 ‐mutant (HBCx‐14) tumor sections. Tumors were collected at day 21. Right panels: Higher magnification images show tumor features from the black boxed area in the left panels. The black arrowhead in the lower right panel indicates a remaining tumor cell. fs: fibrous scar, tc: tumor cells. Scale bars = left panels, 200 μm; right panels, 50 μm. Ratio of fibrous scar area/tumor cell area (sum of fibrous scar area/sum of tumor cell area). Note that combined treatments were much more efficient in replacing tumor cells by fibrous scar. The tumors were collected at day 21 ( n = 4 sections/tumor and 3–4 tumors/group). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P = 0.002, *** P = 0.00008; CDDP versus DMSO or CDDP versus CDDP + PFT‐α). Representative PCR analysis of p53 expression from p53 wild‐type (wt), heterozygous (+/−), and knockout (−/−) mice. The 706‐bp band (neomycin cassette) is detected in p53 +/− and p53 −/− , although not in p53wt mice. By contrast, the 470‐bp band (p53 wild‐type gene) was only detected in p53wt and p53 +/− mice. Representative Western blots using antibodies against p‐p53 (serine 15) and actin in whole cochlear extracts from p53wt mice treated with CDDP for 0, 2, and 5 days. Note the increase in p53 phosphorylation in 2‐ and 5‐day CDDP‐treated cochleae.

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: Intratympanic injection, tumor histology, and p53 genotyping and activation in vivo Shown is the custom‐made microendoscope. It consists of a fiber optic lens (10,000‐pixel resolution) for viewing and one catheter channel equipped with a fine needle for drug delivery. The blue arrowhead indicates the needle. Endoscopic view of the tympanic membrane (left image) and intratympanic injection through a fine needle (right image). The blue arrowhead indicates the needle. Representative scanned images of hematoxylin–eosin–safranin‐stained TP53 ‐mutant (HBCx‐14) tumor sections. Tumors were collected at day 21. Right panels: Higher magnification images show tumor features from the black boxed area in the left panels. The black arrowhead in the lower right panel indicates a remaining tumor cell. fs: fibrous scar, tc: tumor cells. Scale bars = left panels, 200 μm; right panels, 50 μm. Ratio of fibrous scar area/tumor cell area (sum of fibrous scar area/sum of tumor cell area). Note that combined treatments were much more efficient in replacing tumor cells by fibrous scar. The tumors were collected at day 21 ( n = 4 sections/tumor and 3–4 tumors/group). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P = 0.002, *** P = 0.00008; CDDP versus DMSO or CDDP versus CDDP + PFT‐α). Representative PCR analysis of p53 expression from p53 wild‐type (wt), heterozygous (+/−), and knockout (−/−) mice. The 706‐bp band (neomycin cassette) is detected in p53 +/− and p53 −/− , although not in p53wt mice. By contrast, the 470‐bp band (p53 wild‐type gene) was only detected in p53wt and p53 +/− mice. Representative Western blots using antibodies against p‐p53 (serine 15) and actin in whole cochlear extracts from p53wt mice treated with CDDP for 0, 2, and 5 days. Note the increase in p53 phosphorylation in 2‐ and 5‐day CDDP‐treated cochleae.

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Injection, Activation Assay, In Vivo, Staining, Mutagenesis, Polymerase Chain Reaction, Expressing, Knock-Out, Mouse Assay, Western Blot

    Effects of CDDP treatment on the DNA damage pathways, and ATM and p53 inhibition Representative PCR analysis of mATR and mChk1 expression in cochleae, testis, and kidney tissues from P3 mice. Water was used as a negative control. Representative Western blot analysis showing the level of Chk1 phosphorylation in protein extracts from cultured whole cochleae treated or not with 10 μM CDDP and from control and UV light‐exposed mouse embryonic fibroblasts (MEF). 3D images showing IHC and OHC nuclei from the basal region of the organ of Corti cultures treated with medium alone (control) or 10 μM CDDP for 1 day and immunolabeled for p‐ATM (green in C) or p‐Chk2 (green in D). Scale bar = 5 μm. 3D images showing OHC nuclei from the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for p‐ATM (green). Scale bar = 5 μm. Quantification of p‐ATM foci number per nucleus in both inner (red bars) and outer (blue bars) hair cells for all treatment conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P ≤ 0.008, *** P ≤ 0.0006; CDDP versus control or CDDP versus CDDP + KU55933). Confocal images showing the basal region of organ of Corti cultures treated with medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the levels of surviving IHCs (red bars) and OHCs (blue bars) for all conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.02, ** P ≤ 0.006, *** P = 0.0004; CDDP versus control, or CDDP versus CDDP + PFT‐α). Data information: All experiments were performed in triplicate.

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: Effects of CDDP treatment on the DNA damage pathways, and ATM and p53 inhibition Representative PCR analysis of mATR and mChk1 expression in cochleae, testis, and kidney tissues from P3 mice. Water was used as a negative control. Representative Western blot analysis showing the level of Chk1 phosphorylation in protein extracts from cultured whole cochleae treated or not with 10 μM CDDP and from control and UV light‐exposed mouse embryonic fibroblasts (MEF). 3D images showing IHC and OHC nuclei from the basal region of the organ of Corti cultures treated with medium alone (control) or 10 μM CDDP for 1 day and immunolabeled for p‐ATM (green in C) or p‐Chk2 (green in D). Scale bar = 5 μm. 3D images showing OHC nuclei from the basal region of the organ of Corti cultures treated with medium alone, 10 μM KU55933, 10 μM CDDP, or 10 μM CDDP in combination with 10 μM KU55933 for 1 day and immunolabeled for p‐ATM (green). Scale bar = 5 μm. Quantification of p‐ATM foci number per nucleus in both inner (red bars) and outer (blue bars) hair cells for all treatment conditions ( n = 50 nuclei per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (** P ≤ 0.008, *** P ≤ 0.0006; CDDP versus control or CDDP versus CDDP + KU55933). Confocal images showing the basal region of organ of Corti cultures treated with medium alone, 100 μM PFT‐α, 10 μM CDDP, or 10 μM CDDP in combination with 100 μM PFT‐α for 5 days and immunolabeled for myosin 7A (red). Scale bar = 24 μm. Histograms representing the levels of surviving IHCs (red bars) and OHCs (blue bars) for all conditions after 5 days ( n = 5 cochleae per condition and per time point). Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (* P = 0.02, ** P ≤ 0.006, *** P = 0.0004; CDDP versus control, or CDDP versus CDDP + PFT‐α). Data information: All experiments were performed in triplicate.

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Inhibition, Polymerase Chain Reaction, Expressing, Mouse Assay, Negative Control, Western Blot, Cell Culture, Immunohistochemistry, Immunolabeling

    Genetic and pharmacological deletion of p53 prevents loss of hearing and hair cells in adult mice Representative auditory brainstem response (ABR) waveforms evoked by 16 kHz tone bursts in p53wt mice treated with saline (black plot) or CDDP (green plot), and p53 −/− mice treated with saline (light blue plot) or CDDP (dark blue plot) for 5 days. ABR thresholds recorded in p53wt mice before (gray plot) and after 5 days of saline (black plot) or CDDP treatments (green plot), and ABR thresholds recorded in p53 −/− mice before (light gray plot), and after 5 days of saline (light blue plot) or CDDP treatment (dark blue plot). Saline‐treated group: n = 7; CDDP‐treated group: n = 12. Mean ABR threshold from 4 kHz to 32 kHz derived from (B). One‐way ANOVA test followed by post hoc Tukey's test (** P ≤ 0.008; p53wt + CDDP, d5 versus p53wt, before or p53wt + CDDP, d5 versus p53 −/− + CDDP, d5). Representative scanning electron microscopy micrographs showing the basal regions of cochleae from CDDP‐treated p53wt and p53 −/− mice after 5 days. Scale bar = 15 μm. Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apex provided from saline‐treated p53wt mice (black bars), CDDP‐treated p53wt mice (green bars), or p53 −/− mice (blue bars), after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008, p53wt + CDDP, d5 versus p53wt + saline, d5 or p53wt + CDDP, d5 versus p53 −/− + CDDP, d5). ABR thresholds from p53wt mice recorded prior to (gray plot) or after 5 days systemic treatment with: DMSO (yellow plot), CDDP + DMSO (green plot), CDDP + PFT‐α (pink plot). DMSO‐treated group: n = 7; CDDP + DMSO‐treated group: n = 12; CDDP + PFT‐α‐treated group: n = 12. Mean ABR threshold from 4 to 32 kHz derived from (F). One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0005; CDDP + DMSO, d5 versus before or CDDP + DMSO, d5 versus CDDP + PFT‐α, d5). Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apical end taken from p53wt mice treated with: DMSO (yellow bars), CDDP + DMSO (green bars), CDDP + PFT‐α (pink bars), after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP + DMSO, d5 versus DMSO, d5 or CDDP + DMSO, d5 versus CDDP + PFT‐α, d5). ABR thresholds from p53wt mice recorded prior to (gray plot and black plot for left and right ear, respectively) or after 5 days of systemic treatment with CDDP plus intratympanic injection of DMSO into the left ear (green plot) and of PFT‐α into the right ear (pink plot). n = 14 per group. Mean ABR threshold from 4 to 32 kHz derived from (I) ( n = 14). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0003; CDDP + left ear, DMSO versus before, left ear or CDDP + left ear, DMSO versus CDDP + right ear, PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apical end taken from the DMSO‐treated left ear (green bars) and PFT‐α‐treated right ear (pink bars) of the same CDDP‐treated p53wt mice after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP + right ear, PFT‐α versus CDDP + left ear, DMSO). Data information: Data are expressed as mean ± SEM.

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: Genetic and pharmacological deletion of p53 prevents loss of hearing and hair cells in adult mice Representative auditory brainstem response (ABR) waveforms evoked by 16 kHz tone bursts in p53wt mice treated with saline (black plot) or CDDP (green plot), and p53 −/− mice treated with saline (light blue plot) or CDDP (dark blue plot) for 5 days. ABR thresholds recorded in p53wt mice before (gray plot) and after 5 days of saline (black plot) or CDDP treatments (green plot), and ABR thresholds recorded in p53 −/− mice before (light gray plot), and after 5 days of saline (light blue plot) or CDDP treatment (dark blue plot). Saline‐treated group: n = 7; CDDP‐treated group: n = 12. Mean ABR threshold from 4 kHz to 32 kHz derived from (B). One‐way ANOVA test followed by post hoc Tukey's test (** P ≤ 0.008; p53wt + CDDP, d5 versus p53wt, before or p53wt + CDDP, d5 versus p53 −/− + CDDP, d5). Representative scanning electron microscopy micrographs showing the basal regions of cochleae from CDDP‐treated p53wt and p53 −/− mice after 5 days. Scale bar = 15 μm. Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apex provided from saline‐treated p53wt mice (black bars), CDDP‐treated p53wt mice (green bars), or p53 −/− mice (blue bars), after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008, p53wt + CDDP, d5 versus p53wt + saline, d5 or p53wt + CDDP, d5 versus p53 −/− + CDDP, d5). ABR thresholds from p53wt mice recorded prior to (gray plot) or after 5 days systemic treatment with: DMSO (yellow plot), CDDP + DMSO (green plot), CDDP + PFT‐α (pink plot). DMSO‐treated group: n = 7; CDDP + DMSO‐treated group: n = 12; CDDP + PFT‐α‐treated group: n = 12. Mean ABR threshold from 4 to 32 kHz derived from (F). One‐way ANOVA test followed by post hoc Tukey's test (*** P ≤ 0.0005; CDDP + DMSO, d5 versus before or CDDP + DMSO, d5 versus CDDP + PFT‐α, d5). Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apical end taken from p53wt mice treated with: DMSO (yellow bars), CDDP + DMSO (green bars), CDDP + PFT‐α (pink bars), after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP + DMSO, d5 versus DMSO, d5 or CDDP + DMSO, d5 versus CDDP + PFT‐α, d5). ABR thresholds from p53wt mice recorded prior to (gray plot and black plot for left and right ear, respectively) or after 5 days of systemic treatment with CDDP plus intratympanic injection of DMSO into the left ear (green plot) and of PFT‐α into the right ear (pink plot). n = 14 per group. Mean ABR threshold from 4 to 32 kHz derived from (I) ( n = 14). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0003; CDDP + left ear, DMSO versus before, left ear or CDDP + left ear, DMSO versus CDDP + right ear, PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in four cochlear regions located at 1.1, 2.6, 3.5, or 4.1 mm from the cochlear apical end taken from the DMSO‐treated left ear (green bars) and PFT‐α‐treated right ear (pink bars) of the same CDDP‐treated p53wt mice after 5 days ( n = 5 per group). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP + right ear, PFT‐α versus CDDP + left ear, DMSO). Data information: Data are expressed as mean ± SEM.

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Mouse Assay, Derivative Assay, Electron Microscopy, Injection

    PFT‐α enhances CDDP‐induced anti‐angiogenesis and suppresses autophagy selectively in TP53‐ mutant tumors Representative confocal images of microvessels in transversal tumor sections from HBCx‐14 ( TP53 ‐mutant) tumors treated with either DMSO, CDDP, or a combination of CDDP and PFT‐α. The sections were immunolabeled for CD31 (red) and viewed with a 20× objective. The basal‐like breast cancer cells were immunolabeled in green with an antibody against cytokeratin 5 and 8. Upper right panel is a 2D projection from the white boxed area in upper left panel. The red area corresponds to CD31‐labeled endothelial area, and the white area represents the lumen area. The white line shows the vessel perimeter. Scale bars = left panels, 50 μm; right panels, 35 μm. The tumor samples were collected at day 21. Histograms representing the percentage of vascular area calculated using 2D reconstruction image analysis and the formula: vessel/vascular area = area of CD31‐positive objects + lumen area per field area × 100%. Both HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors from the different treated groups were collected at day 21 ( n = 4 sections/tumor and 3–4 tumors/group). Data are expressed as mean ± SEM. Kruskal–Wallis test followed by post hoc Dunn's test (*** P ≤ 0.0004; CDDP versus DMSO or CDDP versus CDDP + PFT‐α). Representative confocal images of cleaved caspase‐3‐positive cells (red) in the transversal tumor sections and viewed with a 20× objective. The stromal compartments were immunolabeled in green with an antibody against vimentin. HBCx‐14 ( TP53 ‐mutant) tumors from the different treated groups were collected at day 18. Scale bar = 50 μm. c‐cas‐3: cleaved caspase‐3. Representative Western blot analysis using antibodies against β‐actin, p53, and p21 in tumor extracts from HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors treated with either DMSO or CDDP and collected at day 18. Note the higher CDDP‐induced increase in p53 and p21 expression in TP53 wt HBCx‐90 tumors. Representative Western blot analysis using antibodies against β‐actin, p‐Chk1, Beclin 1, LC3‐I/II, and Rab7 in tumor extracts from HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors treated with either DMSO, PFT‐α, CDDP, or a combination of CDDP and PFT‐α. The tumor samples were collected at day 18. Histograms representing the levels of Beclin 1, LC3‐II, and Rab7 in HBCx‐14 and HBCx‐90 tumors treated with the different regimens ( n = 3–4 tumors per group, all experiments were performed in triplicate). Actin served as a loading control. Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (G: * P = 0.03, ** P = 0.006, *** P ≤ 0.0004; H: * P = 0.02, *** P = 0.0005; I: * P = 0.03, *** P ≤ 0.0006; CDDP versus DMSO or CDDP versus CDDP + PFT‐α).

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: PFT‐α enhances CDDP‐induced anti‐angiogenesis and suppresses autophagy selectively in TP53‐ mutant tumors Representative confocal images of microvessels in transversal tumor sections from HBCx‐14 ( TP53 ‐mutant) tumors treated with either DMSO, CDDP, or a combination of CDDP and PFT‐α. The sections were immunolabeled for CD31 (red) and viewed with a 20× objective. The basal‐like breast cancer cells were immunolabeled in green with an antibody against cytokeratin 5 and 8. Upper right panel is a 2D projection from the white boxed area in upper left panel. The red area corresponds to CD31‐labeled endothelial area, and the white area represents the lumen area. The white line shows the vessel perimeter. Scale bars = left panels, 50 μm; right panels, 35 μm. The tumor samples were collected at day 21. Histograms representing the percentage of vascular area calculated using 2D reconstruction image analysis and the formula: vessel/vascular area = area of CD31‐positive objects + lumen area per field area × 100%. Both HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors from the different treated groups were collected at day 21 ( n = 4 sections/tumor and 3–4 tumors/group). Data are expressed as mean ± SEM. Kruskal–Wallis test followed by post hoc Dunn's test (*** P ≤ 0.0004; CDDP versus DMSO or CDDP versus CDDP + PFT‐α). Representative confocal images of cleaved caspase‐3‐positive cells (red) in the transversal tumor sections and viewed with a 20× objective. The stromal compartments were immunolabeled in green with an antibody against vimentin. HBCx‐14 ( TP53 ‐mutant) tumors from the different treated groups were collected at day 18. Scale bar = 50 μm. c‐cas‐3: cleaved caspase‐3. Representative Western blot analysis using antibodies against β‐actin, p53, and p21 in tumor extracts from HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors treated with either DMSO or CDDP and collected at day 18. Note the higher CDDP‐induced increase in p53 and p21 expression in TP53 wt HBCx‐90 tumors. Representative Western blot analysis using antibodies against β‐actin, p‐Chk1, Beclin 1, LC3‐I/II, and Rab7 in tumor extracts from HBCx‐14 ( TP53 ‐mutant) and HBCx‐90 ( TP53 wt) tumors treated with either DMSO, PFT‐α, CDDP, or a combination of CDDP and PFT‐α. The tumor samples were collected at day 18. Histograms representing the levels of Beclin 1, LC3‐II, and Rab7 in HBCx‐14 and HBCx‐90 tumors treated with the different regimens ( n = 3–4 tumors per group, all experiments were performed in triplicate). Actin served as a loading control. Data are expressed as mean ± SEM. One‐way ANOVA test followed by post hoc Tukey's test (G: * P = 0.03, ** P = 0.006, *** P ≤ 0.0004; H: * P = 0.02, *** P = 0.0005; I: * P = 0.03, *** P ≤ 0.0006; CDDP versus DMSO or CDDP versus CDDP + PFT‐α).

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Mutagenesis, Immunolabeling, Labeling, Western Blot, Expressing

    PFT‐α protects cochlea from ototoxicity without compromising and even enhancing CDDP anti‐tumor efficacy in patient‐derived breast cancer xenograft mice ABR thresholds recorded prior to (gray plot) or at day 28 in HBCx‐90 ( TP53 wt)‐bearing mice received systemic treatment with: DMSO (black plot), PFT‐α (yellow plot), CDDP (green plot), CDDP + PFT‐α (pink plot). Before: n = 20; DMSO: n = 5; PFT‐α: n = 5; CDDP: n = 5; CDDP + PFT‐α: n = 5. Mean ABR threshold from 4 to 32 kHz derived from (A). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0002; CDDP versus before, CDDP versus CDDP + PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in three cochlear regions located at 1.1, 2.6, and 3.5 mm from the cochlear apical end. These cochleae ( n = 5 per group) were collected at 28 days from the beginning of treatment with DMSO (black bars), PFT‐α (yellow bars), CDDP (green bars), or CDDP + PFT‐α (pink bars). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.007; CDDP, d28 versus DMSO, d28 or CDDP, d28 versus CDDP + PFT‐α, d28). Tumor growth curves alongside images of dissected tumors collected on day 28. Note the partial inhibition of growth in CDDP and CDDP + PFT‐α‐treated mice. 0, 5, 7 and 14 days: DMSO‐ or PFT‐α‐treated group: n = 10; CDDP‐ or CDDP + PFT‐α‐treated group: n = 11. 21 days: DMSO‐ or PFT‐α‐treated group: n = 7; CDDP‐ or CDDP + PFT‐α‐treated group: n = 8. 28 days: n = 5 per group. ABR thresholds recorded prior to (gray plot) or at day 35 in HBCx‐14 ( TP53 ‐mutant)‐bearing mice received systemic treatment with DMSO (black plot), PFT‐α (yellow plot), CDDP (green plot), CDDP + PFT‐α (pink plot). Before: n = 30; DMSO: n = 5; PFT‐α: n = 5; CDDP: n = 10; CDDP + PFT‐α: n = 10. Mean ABR threshold from 4 kHz to 32 kHz derived from (E). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0003; CDDP versus before or CDDP versus CDDP + PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in three cochlear regions located at 1.1, 2.6, and 3.5 mm from the cochlear apical end. These cochleae ( n = 5 per group) were collected at 35 days from the beginning of treatment with DMSO (black bars), PFT‐α (yellow bars), CDDP (green bars), or CDDP + PFT‐α (pink bars). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP, d35 versus DMSO, d35 or CDDP, d35 versus CDDP + PFT‐α, d35). Tumor growth curves alongside images of dissected tumors collected on day 35. Note the complete disappearance of tumors at day 35 and the significantly reduced tumor regrowth up to day 70 in CDDP + PFT‐α‐treated mice. 0, 7 and 14 days: DMSO‐ or PFT‐α‐treated group: n = 11; CDDP‐treated group: n = 16; CDDP + PFT‐α‐treated group: n = 17. 21 days: DMSO‐ or PFT‐α‐treated group: n = 8; CDDP‐treated group: n = 13; CDDP + PFT‐α‐treated group: n = 14. 35 days: DMSO‐ or PFT‐α‐treated group: n = 5; CDDP‐treated group: n = 10; CDDP + PFT‐α‐treated group: n = 10. 42, 56 and 70 days: CDDP‐ or CDDP + PFT‐α‐treated group n = 5 per group. Data information: Data are expressed as mean ± SEM.

    Journal: EMBO Molecular Medicine

    Article Title: Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy

    doi: 10.15252/emmm.201606230

    Figure Lengend Snippet: PFT‐α protects cochlea from ototoxicity without compromising and even enhancing CDDP anti‐tumor efficacy in patient‐derived breast cancer xenograft mice ABR thresholds recorded prior to (gray plot) or at day 28 in HBCx‐90 ( TP53 wt)‐bearing mice received systemic treatment with: DMSO (black plot), PFT‐α (yellow plot), CDDP (green plot), CDDP + PFT‐α (pink plot). Before: n = 20; DMSO: n = 5; PFT‐α: n = 5; CDDP: n = 5; CDDP + PFT‐α: n = 5. Mean ABR threshold from 4 to 32 kHz derived from (A). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0002; CDDP versus before, CDDP versus CDDP + PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in three cochlear regions located at 1.1, 2.6, and 3.5 mm from the cochlear apical end. These cochleae ( n = 5 per group) were collected at 28 days from the beginning of treatment with DMSO (black bars), PFT‐α (yellow bars), CDDP (green bars), or CDDP + PFT‐α (pink bars). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.007; CDDP, d28 versus DMSO, d28 or CDDP, d28 versus CDDP + PFT‐α, d28). Tumor growth curves alongside images of dissected tumors collected on day 28. Note the partial inhibition of growth in CDDP and CDDP + PFT‐α‐treated mice. 0, 5, 7 and 14 days: DMSO‐ or PFT‐α‐treated group: n = 10; CDDP‐ or CDDP + PFT‐α‐treated group: n = 11. 21 days: DMSO‐ or PFT‐α‐treated group: n = 7; CDDP‐ or CDDP + PFT‐α‐treated group: n = 8. 28 days: n = 5 per group. ABR thresholds recorded prior to (gray plot) or at day 35 in HBCx‐14 ( TP53 ‐mutant)‐bearing mice received systemic treatment with DMSO (black plot), PFT‐α (yellow plot), CDDP (green plot), CDDP + PFT‐α (pink plot). Before: n = 30; DMSO: n = 5; PFT‐α: n = 5; CDDP: n = 10; CDDP + PFT‐α: n = 10. Mean ABR threshold from 4 kHz to 32 kHz derived from (E). One‐way ANOVA test followed by post hoc Tukey's test (*** P = 0.0003; CDDP versus before or CDDP versus CDDP + PFT‐α). Cytocochleograms representing the percentage of surviving hair cells in three cochlear regions located at 1.1, 2.6, and 3.5 mm from the cochlear apical end. These cochleae ( n = 5 per group) were collected at 35 days from the beginning of treatment with DMSO (black bars), PFT‐α (yellow bars), CDDP (green bars), or CDDP + PFT‐α (pink bars). Kruskal–Wallis test followed by post hoc Dunn's test (** P ≤ 0.008; CDDP, d35 versus DMSO, d35 or CDDP, d35 versus CDDP + PFT‐α, d35). Tumor growth curves alongside images of dissected tumors collected on day 35. Note the complete disappearance of tumors at day 35 and the significantly reduced tumor regrowth up to day 70 in CDDP + PFT‐α‐treated mice. 0, 7 and 14 days: DMSO‐ or PFT‐α‐treated group: n = 11; CDDP‐treated group: n = 16; CDDP + PFT‐α‐treated group: n = 17. 21 days: DMSO‐ or PFT‐α‐treated group: n = 8; CDDP‐treated group: n = 13; CDDP + PFT‐α‐treated group: n = 14. 35 days: DMSO‐ or PFT‐α‐treated group: n = 5; CDDP‐treated group: n = 10; CDDP + PFT‐α‐treated group: n = 10. 42, 56 and 70 days: CDDP‐ or CDDP + PFT‐α‐treated group n = 5 per group. Data information: Data are expressed as mean ± SEM.

    Article Snippet: Blots were incubated with mouse monoclonal antibodies against phospho‐Chk1 (1/1,000, Ser345, Cell Signaling Technology, #2348), p53 (1/1,500, Cell Signaling Technology, #2524), and β‐actin (1/10,000, Sigma‐Aldrich, #A1978), and with polyclonal rabbit antibodies against phospho‐H2AX (1/1500, Ser139, Cell Signaling Technology, #2577), phospho‐p53 (1/1500, Ser15, Cell Signaling Technology, #9289), and cleaved caspase‐3 (1/1,000, Asp175, Cell Signaling Technology, #9661), prior to incubation with horseradish peroxidase‐conjugated secondary antibodies (Jackson ImmunoResearch Laboratories, #115‐035‐144 and 111‐035‐144).

    Techniques: Derivative Assay, Mouse Assay, Inhibition, Mutagenesis

    Analysis of telethonin/p53 co-localization

    Journal: Circulation research

    Article Title: Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart

    doi: 10.1161/CIRCRESAHA.111.245787

    Figure Lengend Snippet: Analysis of telethonin/p53 co-localization

    Article Snippet: We used as well p21WAF1 EA10 (Calbiochem), Mdm2 2A9 and 2A10, myc 4A6 (Upstate) and actin AC15 (Abcam), anti-p53 (DO-1, FL 393, Santa Cruz), and/or mouse monoclonal p53 (1C12, Cell signalling), mouse monoclonal anti α-actinin (Sigma) and phalloidin conjugated Alexa 350 antibody.

    Techniques:

    Inhibition of p53 and its effect on telethonin deficiency after TAC and implications for human disease

    Journal: Circulation research

    Article Title: Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart

    doi: 10.1161/CIRCRESAHA.111.245787

    Figure Lengend Snippet: Inhibition of p53 and its effect on telethonin deficiency after TAC and implications for human disease

    Article Snippet: We used as well p21WAF1 EA10 (Calbiochem), Mdm2 2A9 and 2A10, myc 4A6 (Upstate) and actin AC15 (Abcam), anti-p53 (DO-1, FL 393, Santa Cruz), and/or mouse monoclonal p53 (1C12, Cell signalling), mouse monoclonal anti α-actinin (Sigma) and phalloidin conjugated Alexa 350 antibody.

    Techniques: Inhibition

    Telethonin – analysis of fibrosis, apoptosis and p53

    Journal: Circulation research

    Article Title: Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart

    doi: 10.1161/CIRCRESAHA.111.245787

    Figure Lengend Snippet: Telethonin – analysis of fibrosis, apoptosis and p53

    Article Snippet: We used as well p21WAF1 EA10 (Calbiochem), Mdm2 2A9 and 2A10, myc 4A6 (Upstate) and actin AC15 (Abcam), anti-p53 (DO-1, FL 393, Santa Cruz), and/or mouse monoclonal p53 (1C12, Cell signalling), mouse monoclonal anti α-actinin (Sigma) and phalloidin conjugated Alexa 350 antibody.

    Techniques:

    Telethonin/p53 interaction

    Journal: Circulation research

    Article Title: Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart

    doi: 10.1161/CIRCRESAHA.111.245787

    Figure Lengend Snippet: Telethonin/p53 interaction

    Article Snippet: We used as well p21WAF1 EA10 (Calbiochem), Mdm2 2A9 and 2A10, myc 4A6 (Upstate) and actin AC15 (Abcam), anti-p53 (DO-1, FL 393, Santa Cruz), and/or mouse monoclonal p53 (1C12, Cell signalling), mouse monoclonal anti α-actinin (Sigma) and phalloidin conjugated Alexa 350 antibody.

    Techniques:

    Analysis of the effect of telethonin on p53 in vivo

    Journal: Circulation research

    Article Title: Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart

    doi: 10.1161/CIRCRESAHA.111.245787

    Figure Lengend Snippet: Analysis of the effect of telethonin on p53 in vivo

    Article Snippet: We used as well p21WAF1 EA10 (Calbiochem), Mdm2 2A9 and 2A10, myc 4A6 (Upstate) and actin AC15 (Abcam), anti-p53 (DO-1, FL 393, Santa Cruz), and/or mouse monoclonal p53 (1C12, Cell signalling), mouse monoclonal anti α-actinin (Sigma) and phalloidin conjugated Alexa 350 antibody.

    Techniques: In Vivo