p53  (Roche)


Bioz Verified Symbol Roche is a verified supplier
Bioz Manufacturer Symbol Roche manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93

    Structured Review

    Roche p53
    UVB enhances <t>p53</t> mitochondrial translocation (A) C57BL/6 mice were exposed to 5kJ/m 2 of UVB radiation. Whole skin tissue lysates and fractionated mitochondrial lysates were immunoblotted for p53 antibody (DO-1). Ponceau staining was used to confirm equal loading and uniform transfer of protein. Monoclonal anti-β-actin and anti-HSP60 antibodies were used as internal loading control. (B) The p53 accumulations in whole skin lysates and mitochondrial lysates at 1 hr and 24 hr after UVB exposure were quantified. Results were averaged from 3 sets of independent experiments. *P
    P53, supplied by Roche, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p53/product/Roche
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p53 - by Bioz Stars, 2021-06
    93/100 stars

    Images

    1) Product Images from "Manganese superoxide dismutase is a mitochondrial fidelity protein that protects Pol? against UV-induced inactivation"

    Article Title: Manganese superoxide dismutase is a mitochondrial fidelity protein that protects Pol? against UV-induced inactivation

    Journal: Oncogene

    doi: 10.1038/onc.2011.407

    UVB enhances p53 mitochondrial translocation (A) C57BL/6 mice were exposed to 5kJ/m 2 of UVB radiation. Whole skin tissue lysates and fractionated mitochondrial lysates were immunoblotted for p53 antibody (DO-1). Ponceau staining was used to confirm equal loading and uniform transfer of protein. Monoclonal anti-β-actin and anti-HSP60 antibodies were used as internal loading control. (B) The p53 accumulations in whole skin lysates and mitochondrial lysates at 1 hr and 24 hr after UVB exposure were quantified. Results were averaged from 3 sets of independent experiments. *P
    Figure Legend Snippet: UVB enhances p53 mitochondrial translocation (A) C57BL/6 mice were exposed to 5kJ/m 2 of UVB radiation. Whole skin tissue lysates and fractionated mitochondrial lysates were immunoblotted for p53 antibody (DO-1). Ponceau staining was used to confirm equal loading and uniform transfer of protein. Monoclonal anti-β-actin and anti-HSP60 antibodies were used as internal loading control. (B) The p53 accumulations in whole skin lysates and mitochondrial lysates at 1 hr and 24 hr after UVB exposure were quantified. Results were averaged from 3 sets of independent experiments. *P

    Techniques Used: Translocation Assay, Mouse Assay, Staining

    UVB-induced physical interaction of p53-Polγ-mtDNA (A) Skin mitochondrial lysates from wild-type C57BL/6 mice exposed to 5kJ/m 2 of UVB radiation were immunoprecipitated with p53 (DO-1), Polγ antibodies, and control IgG. (B) mtDNA isolated from wild-type C57BL/6 mice skin exposed or sham exposed to 5 kJ/m 2 of UVB radiation was immunoprecipitated with p53 antibody (DO-1) and control IgG. The input mtDNA from control at 1 hr and 24 hr after UVB treatment was used as internal control. Real-Time PCR was used to amplify mtDNA D-loop region from input and immunoprecipitated mtDNA. ***P
    Figure Legend Snippet: UVB-induced physical interaction of p53-Polγ-mtDNA (A) Skin mitochondrial lysates from wild-type C57BL/6 mice exposed to 5kJ/m 2 of UVB radiation were immunoprecipitated with p53 (DO-1), Polγ antibodies, and control IgG. (B) mtDNA isolated from wild-type C57BL/6 mice skin exposed or sham exposed to 5 kJ/m 2 of UVB radiation was immunoprecipitated with p53 antibody (DO-1) and control IgG. The input mtDNA from control at 1 hr and 24 hr after UVB treatment was used as internal control. Real-Time PCR was used to amplify mtDNA D-loop region from input and immunoprecipitated mtDNA. ***P

    Techniques Used: Mouse Assay, Immunoprecipitation, Isolation, Real-time Polymerase Chain Reaction

    UVB-induced physical interaction of MnSOD-p53-Polγ (A) Skin mitochondrial lysates from wild-type C57BL/6 mice exposed to 5kJ/m 2 of UVB radiation were immunoprecipitated with p53 (DO-1), MnSOD antibodies, and control IgG. Co-immunoprecipitated MnSOD and p53 were quantified by immunoblotting with specific antibodies. (B) Co-immunoprecipitation of Polγ and MnSOD. Mitochondrial lysates from mice skin exposed to UVB at 1 hr and 24 hr were immunoprecipitated with Polγ, MnSOD antibodies, and control IgG. Co-immunoprecipitated Polγ and MnSOD were quantified by immunoblotting with specific antibodies. (C) Mitochondrial lysates from p53 +/+ and p53 −/− mice skin exposed to UVB were immunoprecipitated with Polγ, MnSOD antibodies and control IgG. Co-immunoprecipitated Polγ and MnSOD were quantified by immunoblotting with specific antibodies. (D) mtDNA isolated from MnSOD +/+ and MnSOD +/− mice skin exposed to 5kJ/m 2 of UVB radiation was immunoprecipitated with Polγ antibody. Real-time PCR was used to amplify the precipitated mtDNA D-loop. ***P
    Figure Legend Snippet: UVB-induced physical interaction of MnSOD-p53-Polγ (A) Skin mitochondrial lysates from wild-type C57BL/6 mice exposed to 5kJ/m 2 of UVB radiation were immunoprecipitated with p53 (DO-1), MnSOD antibodies, and control IgG. Co-immunoprecipitated MnSOD and p53 were quantified by immunoblotting with specific antibodies. (B) Co-immunoprecipitation of Polγ and MnSOD. Mitochondrial lysates from mice skin exposed to UVB at 1 hr and 24 hr were immunoprecipitated with Polγ, MnSOD antibodies, and control IgG. Co-immunoprecipitated Polγ and MnSOD were quantified by immunoblotting with specific antibodies. (C) Mitochondrial lysates from p53 +/+ and p53 −/− mice skin exposed to UVB were immunoprecipitated with Polγ, MnSOD antibodies and control IgG. Co-immunoprecipitated Polγ and MnSOD were quantified by immunoblotting with specific antibodies. (D) mtDNA isolated from MnSOD +/+ and MnSOD +/− mice skin exposed to 5kJ/m 2 of UVB radiation was immunoprecipitated with Polγ antibody. Real-time PCR was used to amplify the precipitated mtDNA D-loop. ***P

    Techniques Used: Mouse Assay, Immunoprecipitation, Isolation, Real-time Polymerase Chain Reaction

    2) Product Images from "Late recurrence of pStage 1 low-grade serous ovarian tumor presenting as a symptomatic bone metastasis: a case report"

    Article Title: Late recurrence of pStage 1 low-grade serous ovarian tumor presenting as a symptomatic bone metastasis: a case report

    Journal: Diagnostic Pathology

    doi: 10.1186/s13000-018-0720-1

    Photomicrographs of CT-guided needle biopsy of paraspinal neoplasm. a Small uniform columnar or round cells can be seen forming confluent papillae associated with psammoma bodies against a fibrous background (hematoxylin and eosin [HE] stain, × 200). b Neoplastic cells positive for PAX8 (immunohistochemical [IHC] stain, × 200). c Positive for ER (IHC, × 200). d Positive for WT1 (IHC, × 200). e Negative for thyroglobulin (IHC, × 200). f P53 wild-type expression (IHC, × 200)
    Figure Legend Snippet: Photomicrographs of CT-guided needle biopsy of paraspinal neoplasm. a Small uniform columnar or round cells can be seen forming confluent papillae associated with psammoma bodies against a fibrous background (hematoxylin and eosin [HE] stain, × 200). b Neoplastic cells positive for PAX8 (immunohistochemical [IHC] stain, × 200). c Positive for ER (IHC, × 200). d Positive for WT1 (IHC, × 200). e Negative for thyroglobulin (IHC, × 200). f P53 wild-type expression (IHC, × 200)

    Techniques Used: H&E Stain, Immunohistochemistry, Staining, Expressing

    3) Product Images from "A Molecular Stratification of Chilean Gastric Cancer Patients with Potential Clinical Applicability"

    Article Title: A Molecular Stratification of Chilean Gastric Cancer Patients with Potential Clinical Applicability

    Journal: Cancers

    doi: 10.3390/cancers12071863

    Molecular alterations and prognosis by GC subtypes. ( a ) Next Generation Sequencing (NGS) analysis, HER2, PDL1 status, and tumor mutational burden by GC subtype. ( b ) Genomic alterations and p53 status in TP53 mutants versus TP53 wild type. ( c ) Kaplan–Meier plot showing the overall survival by GC subtypes. ( d ) Kaplan–Meier plot comparing OS between TP53 mutants and wild type.
    Figure Legend Snippet: Molecular alterations and prognosis by GC subtypes. ( a ) Next Generation Sequencing (NGS) analysis, HER2, PDL1 status, and tumor mutational burden by GC subtype. ( b ) Genomic alterations and p53 status in TP53 mutants versus TP53 wild type. ( c ) Kaplan–Meier plot showing the overall survival by GC subtypes. ( d ) Kaplan–Meier plot comparing OS between TP53 mutants and wild type.

    Techniques Used: Next-Generation Sequencing

    Proposed molecular stratification system for advanced gastric cancer patients. Briefly, our proposal includes assessment of HER2 and PDL1 status by IHC. Then, patients are stratified according to EBV positivity, MMR, E-cadherin, and p53 status. Whenever possible, we also recommend TP53 analysis. Right panels show representative images for each subtype.
    Figure Legend Snippet: Proposed molecular stratification system for advanced gastric cancer patients. Briefly, our proposal includes assessment of HER2 and PDL1 status by IHC. Then, patients are stratified according to EBV positivity, MMR, E-cadherin, and p53 status. Whenever possible, we also recommend TP53 analysis. Right panels show representative images for each subtype.

    Techniques Used: Immunohistochemistry

    4) Product Images from "Late recurrence of pStage 1 low-grade serous ovarian tumor presenting as a symptomatic bone metastasis: a case report"

    Article Title: Late recurrence of pStage 1 low-grade serous ovarian tumor presenting as a symptomatic bone metastasis: a case report

    Journal: Diagnostic Pathology

    doi: 10.1186/s13000-018-0720-1

    Photomicrographs of CT-guided needle biopsy of paraspinal neoplasm. a Small uniform columnar or round cells can be seen forming confluent papillae associated with psammoma bodies against a fibrous background (hematoxylin and eosin [HE] stain, × 200). b Neoplastic cells positive for PAX8 (immunohistochemical [IHC] stain, × 200). c Positive for ER (IHC, × 200). d Positive for WT1 (IHC, × 200). e Negative for thyroglobulin (IHC, × 200). f P53 wild-type expression (IHC, × 200)
    Figure Legend Snippet: Photomicrographs of CT-guided needle biopsy of paraspinal neoplasm. a Small uniform columnar or round cells can be seen forming confluent papillae associated with psammoma bodies against a fibrous background (hematoxylin and eosin [HE] stain, × 200). b Neoplastic cells positive for PAX8 (immunohistochemical [IHC] stain, × 200). c Positive for ER (IHC, × 200). d Positive for WT1 (IHC, × 200). e Negative for thyroglobulin (IHC, × 200). f P53 wild-type expression (IHC, × 200)

    Techniques Used: H&E Stain, Immunohistochemistry, Staining, Expressing

    5) Product Images from "Overexpression of OATP1B3 confers apoptotic resistance in colon cancer"

    Article Title: Overexpression of OATP1B3 confers apoptotic resistance in colon cancer

    Journal:

    doi: 10.1158/0008-5472.CAN-08-1984

    The overexpression of OATP1B3 conferred a cell survival advantage following Camptothecin (CPT) treatment to cells harboring wildtype p53, but not to cells lacking p53. Cell viability following CPT treatment (10 μM, 24 hrs) was determined using
    Figure Legend Snippet: The overexpression of OATP1B3 conferred a cell survival advantage following Camptothecin (CPT) treatment to cells harboring wildtype p53, but not to cells lacking p53. Cell viability following CPT treatment (10 μM, 24 hrs) was determined using

    Techniques Used: Over Expression, Cycling Probe Technology

    The overexpression of OATP1B3 in HCT-116 p53+/+ cells provided apoptotic resistance following Camptothecin (CPT) treatment. A: HCT-116 p53+/+ cells stably transfected with OATP1B3 or the empty vector were treated with CPT (10 μM, 24 hrs). Apoptotic
    Figure Legend Snippet: The overexpression of OATP1B3 in HCT-116 p53+/+ cells provided apoptotic resistance following Camptothecin (CPT) treatment. A: HCT-116 p53+/+ cells stably transfected with OATP1B3 or the empty vector were treated with CPT (10 μM, 24 hrs). Apoptotic

    Techniques Used: Over Expression, Cycling Probe Technology, Stable Transfection, Transfection, Plasmid Preparation

    Co-expression of OATP1B3 affects p53 transcriptional activity. A: The results from the p53-responsive PG13-luc and P21WAF1-luc reporter assays in HCT-116 p53-/- cells demonstrate that OATP1B3 expression causes a decrease in the transcriptional activity
    Figure Legend Snippet: Co-expression of OATP1B3 affects p53 transcriptional activity. A: The results from the p53-responsive PG13-luc and P21WAF1-luc reporter assays in HCT-116 p53-/- cells demonstrate that OATP1B3 expression causes a decrease in the transcriptional activity

    Techniques Used: Expressing, Activity Assay

    The OATP1B3 variant (G583E) lacking the transport activity confers neither an inhibitory effect on p53 transcriptional activity nor a survival advantage following CPT treatment. A: The results from the p53-responsive PG13-luc reporter assays in HCT-116
    Figure Legend Snippet: The OATP1B3 variant (G583E) lacking the transport activity confers neither an inhibitory effect on p53 transcriptional activity nor a survival advantage following CPT treatment. A: The results from the p53-responsive PG13-luc reporter assays in HCT-116

    Techniques Used: Variant Assay, Activity Assay, Cycling Probe Technology

    6) Product Images from "A living biobank of ovarian cancer ex vivo models reveals profound mitotic heterogeneity"

    Article Title: A living biobank of ovarian cancer ex vivo models reveals profound mitotic heterogeneity

    Journal: Nature Communications

    doi: 10.1038/s41467-020-14551-2

    Characterisation of ex vivo models. a Phase contrast images showing distinct morphologies of stromal and tumour cells. Scale bar, 200 µm. b Time-lapse imaging measuring confluency showing suppression of proliferation by 1 µM cisplatin and 100 nM paclitaxel. c Immunofluorescence images showing expression of PAX8 and Ki67. Scale bar, 50 µm. d Flow cytometry profiles quantitating the tumour markers EpCAM and CA125, and the stromal markers CD44 and CD105. Numbers represent percentage of cells in the quadrant. e Immunofluorescence images of Nutlin-3-treated cells (OCM.79) showing stabilisation of p53 in stromal cells but not tumour, and DNA sequence showing TP53 mutation in tumour cells (OCM.38a). Scale bar, 20 µm. Data in panels a and c are derived from analysis of OCM.79, while data in panels b and d are derived from analysis of OCMs 38a, and 66-5 respectively. Panels a , c and e are representative images from single experiments. Source data for panels b , c and d are provided as a Source Data file, including the gating/sorting strategy for panel d . See also Supplementary Figs. 1 and 2 .
    Figure Legend Snippet: Characterisation of ex vivo models. a Phase contrast images showing distinct morphologies of stromal and tumour cells. Scale bar, 200 µm. b Time-lapse imaging measuring confluency showing suppression of proliferation by 1 µM cisplatin and 100 nM paclitaxel. c Immunofluorescence images showing expression of PAX8 and Ki67. Scale bar, 50 µm. d Flow cytometry profiles quantitating the tumour markers EpCAM and CA125, and the stromal markers CD44 and CD105. Numbers represent percentage of cells in the quadrant. e Immunofluorescence images of Nutlin-3-treated cells (OCM.79) showing stabilisation of p53 in stromal cells but not tumour, and DNA sequence showing TP53 mutation in tumour cells (OCM.38a). Scale bar, 20 µm. Data in panels a and c are derived from analysis of OCM.79, while data in panels b and d are derived from analysis of OCMs 38a, and 66-5 respectively. Panels a , c and e are representative images from single experiments. Source data for panels b , c and d are provided as a Source Data file, including the gating/sorting strategy for panel d . See also Supplementary Figs. 1 and 2 .

    Techniques Used: Ex Vivo, Imaging, Immunofluorescence, Expressing, Flow Cytometry, Sequencing, Mutagenesis, Derivative Assay

    7) Product Images from "LonP1 Differently Modulates Mitochondrial Function and Bioenergetics of Primary Versus Metastatic Colon Cancer Cells"

    Article Title: LonP1 Differently Modulates Mitochondrial Function and Bioenergetics of Primary Versus Metastatic Colon Cancer Cells

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2018.00254

    LonP1 upregulation is associated with mutated p53 or nuclear β-ctn. (A) Representative immunohistochemical stainings of Ki-67, membrane β-ctn (m-βctn), nuclear β-ctn (n-βctn), and p53 in colorectal cancer (CRC) tissues. (B) Association between expression of LonP1, mutated p53, non-mutated p53, membrane β-ctn, or nuclear β-ctn in CRC tissues; * P
    Figure Legend Snippet: LonP1 upregulation is associated with mutated p53 or nuclear β-ctn. (A) Representative immunohistochemical stainings of Ki-67, membrane β-ctn (m-βctn), nuclear β-ctn (n-βctn), and p53 in colorectal cancer (CRC) tissues. (B) Association between expression of LonP1, mutated p53, non-mutated p53, membrane β-ctn, or nuclear β-ctn in CRC tissues; * P

    Techniques Used: Immunohistochemistry, Expressing

    8) Product Images from "The Predictive Value of Pathologic Features in Pituitary Adenoma and Correlation with Pituitary Adenoma Recurrence"

    Article Title: The Predictive Value of Pathologic Features in Pituitary Adenoma and Correlation with Pituitary Adenoma Recurrence

    Journal: Journal of Pathology and Translational Medicine

    doi: 10.4132/jptm.2016.06.30

    Microscopic findings of an atypical pituitary adenoma case with sphenoid sinus and dura invasion. (A) Tumor cells invading the sphenoid sinus. (B) Foci of tumor cell infiltration into the dura. (C) Tumor cells show extensive p53 immunoreactivity. (D) High Ki-67 labeling index (about 40%) is noted.
    Figure Legend Snippet: Microscopic findings of an atypical pituitary adenoma case with sphenoid sinus and dura invasion. (A) Tumor cells invading the sphenoid sinus. (B) Foci of tumor cell infiltration into the dura. (C) Tumor cells show extensive p53 immunoreactivity. (D) High Ki-67 labeling index (about 40%) is noted.

    Techniques Used: Labeling

    9) Product Images from "Involvement of c-Abl, p53 and the MAP kinase JNK in the cell death program initiated in A2E-laden ARPE-19 cells by exposure to blue light"

    Article Title: Involvement of c-Abl, p53 and the MAP kinase JNK in the cell death program initiated in A2E-laden ARPE-19 cells by exposure to blue light

    Journal: Apoptosis : an international journal on programmed cell death

    doi: 10.1007/s10495-008-0285-7

    Blue light exposure of A2E-laden ARPE-19 cells increases p53-, but not Bax-, protein expression. a A2E-laden ARPE-19 cells were irradiated for 20 min (A2E + 430 nm). Controls were A2E-free cells irradiated at 430 nm (430 nm) and cells that had only accumulated
    Figure Legend Snippet: Blue light exposure of A2E-laden ARPE-19 cells increases p53-, but not Bax-, protein expression. a A2E-laden ARPE-19 cells were irradiated for 20 min (A2E + 430 nm). Controls were A2E-free cells irradiated at 430 nm (430 nm) and cells that had only accumulated

    Techniques Used: Expressing, Irradiation

    Silencing p53 by transfection with specific oligonucleotide and siRNA protects ARPE-19 cells against cell death induced by blue light irradiation of A2E-laden ARPE-19 cells. a A2E-laden ARPE-19 cells (A2E) were untransfected or transfected with a specific
    Figure Legend Snippet: Silencing p53 by transfection with specific oligonucleotide and siRNA protects ARPE-19 cells against cell death induced by blue light irradiation of A2E-laden ARPE-19 cells. a A2E-laden ARPE-19 cells (A2E) were untransfected or transfected with a specific

    Techniques Used: Transfection, Irradiation

    10) Product Images from "BAX/BAK-Independent Mitoptosis during Cell Death Induced by Proteasome Inhibition?"

    Article Title: BAX/BAK-Independent Mitoptosis during Cell Death Induced by Proteasome Inhibition?

    Journal:

    doi: 10.1158/1541-7786.MCR-08-0183

    Effect of protein synthesis inhibition and siRNA-mediated knockdown of BH3-only proteins and p53. A . Western blot analysis of protein levels. HCT116 Bax −/− cells were treated with cycloheximide ( CHX ), DMSO, and MG132 alone or in combination
    Figure Legend Snippet: Effect of protein synthesis inhibition and siRNA-mediated knockdown of BH3-only proteins and p53. A . Western blot analysis of protein levels. HCT116 Bax −/− cells were treated with cycloheximide ( CHX ), DMSO, and MG132 alone or in combination

    Techniques Used: Inhibition, Western Blot

    Effect of coexpression of BH3-only proteins and p53 on cell death in HCT 116 cells. A . Colony survival assay. Indicated HCT116 cell lines were either mock transfected or transfected with empty vector or vectors expressing various proteins together or
    Figure Legend Snippet: Effect of coexpression of BH3-only proteins and p53 on cell death in HCT 116 cells. A . Colony survival assay. Indicated HCT116 cell lines were either mock transfected or transfected with empty vector or vectors expressing various proteins together or

    Techniques Used: Clonogenic Cell Survival Assay, Transfection, Plasmid Preparation, Expressing

    Effect of MG132 on expression of BCL-2-family proteins and p53. A . Western blot analysis of HCT116 wt, Bax −/− , or p53 −/− cells 24 h after MG132 treatment. B . Time-course analysis of protein levels during MG132 treatment.
    Figure Legend Snippet: Effect of MG132 on expression of BCL-2-family proteins and p53. A . Western blot analysis of HCT116 wt, Bax −/− , or p53 −/− cells 24 h after MG132 treatment. B . Time-course analysis of protein levels during MG132 treatment.

    Techniques Used: Expressing, Western Blot

    Mitochondrial association of BH3-only proteins and p53 and effect on MMP. A . Western blot analysis of cytochrome c ( Cyt c ) and AIF. The cytosolic and mitochondrial fractions of DMSO- or MG132-treated HCT116 Bax −/ − cells 6 h after exposure
    Figure Legend Snippet: Mitochondrial association of BH3-only proteins and p53 and effect on MMP. A . Western blot analysis of cytochrome c ( Cyt c ) and AIF. The cytosolic and mitochondrial fractions of DMSO- or MG132-treated HCT116 Bax −/ − cells 6 h after exposure

    Techniques Used: Western Blot

    BAX- and p53-independent cell death by MG132. A . Representative light microscopic images (×120) of HCT116 wt, Bax −/− , or p53 −/− cells 24 h after treatment with DMSO or MG132. B . The cell viability was determined
    Figure Legend Snippet: BAX- and p53-independent cell death by MG132. A . Representative light microscopic images (×120) of HCT116 wt, Bax −/− , or p53 −/− cells 24 h after treatment with DMSO or MG132. B . The cell viability was determined

    Techniques Used:

    11) Product Images from "A living biobank of ovarian cancer ex vivo models reveals profound mitotic heterogeneity"

    Article Title: A living biobank of ovarian cancer ex vivo models reveals profound mitotic heterogeneity

    Journal: Nature Communications

    doi: 10.1038/s41467-020-14551-2

    Characterisation of ex vivo models. a Phase contrast images showing distinct morphologies of stromal and tumour cells. Scale bar, 200 µm. b Time-lapse imaging measuring confluency showing suppression of proliferation by 1 µM cisplatin and 100 nM paclitaxel. c Immunofluorescence images showing expression of PAX8 and Ki67. Scale bar, 50 µm. d Flow cytometry profiles quantitating the tumour markers EpCAM and CA125, and the stromal markers CD44 and CD105. Numbers represent percentage of cells in the quadrant. e Immunofluorescence images of Nutlin-3-treated cells (OCM.79) showing stabilisation of p53 in stromal cells but not tumour, and DNA sequence showing TP53 mutation in tumour cells (OCM.38a). Scale bar, 20 µm. Data in panels a and c are derived from analysis of OCM.79, while data in panels b and d are derived from analysis of OCMs 38a, and 66-5 respectively. Panels a , c and e are representative images from single experiments. Source data for panels b , c and d are provided as a Source Data file, including the gating/sorting strategy for panel d . See also Supplementary Figs. 1 and 2 .
    Figure Legend Snippet: Characterisation of ex vivo models. a Phase contrast images showing distinct morphologies of stromal and tumour cells. Scale bar, 200 µm. b Time-lapse imaging measuring confluency showing suppression of proliferation by 1 µM cisplatin and 100 nM paclitaxel. c Immunofluorescence images showing expression of PAX8 and Ki67. Scale bar, 50 µm. d Flow cytometry profiles quantitating the tumour markers EpCAM and CA125, and the stromal markers CD44 and CD105. Numbers represent percentage of cells in the quadrant. e Immunofluorescence images of Nutlin-3-treated cells (OCM.79) showing stabilisation of p53 in stromal cells but not tumour, and DNA sequence showing TP53 mutation in tumour cells (OCM.38a). Scale bar, 20 µm. Data in panels a and c are derived from analysis of OCM.79, while data in panels b and d are derived from analysis of OCMs 38a, and 66-5 respectively. Panels a , c and e are representative images from single experiments. Source data for panels b , c and d are provided as a Source Data file, including the gating/sorting strategy for panel d . See also Supplementary Figs. 1 and 2 .

    Techniques Used: Ex Vivo, Imaging, Immunofluorescence, Expressing, Flow Cytometry, Sequencing, Mutagenesis, Derivative Assay

    12) Product Images from "Involvement of c-Abl, p53 and the MAP kinase JNK in the cell death program initiated in A2E-laden ARPE-19 cells by exposure to blue light"

    Article Title: Involvement of c-Abl, p53 and the MAP kinase JNK in the cell death program initiated in A2E-laden ARPE-19 cells by exposure to blue light

    Journal: Apoptosis : an international journal on programmed cell death

    doi: 10.1007/s10495-008-0285-7

    Blue light exposure of A2E-laden ARPE-19 cells increases p53-, but not Bax-, protein expression. a A2E-laden ARPE-19 cells were irradiated for 20 min (A2E + 430 nm). Controls were A2E-free cells irradiated at 430 nm (430 nm) and cells that had only accumulated
    Figure Legend Snippet: Blue light exposure of A2E-laden ARPE-19 cells increases p53-, but not Bax-, protein expression. a A2E-laden ARPE-19 cells were irradiated for 20 min (A2E + 430 nm). Controls were A2E-free cells irradiated at 430 nm (430 nm) and cells that had only accumulated

    Techniques Used: Expressing, Irradiation

    Silencing p53 by transfection with specific oligonucleotide and siRNA protects ARPE-19 cells against cell death induced by blue light irradiation of A2E-laden ARPE-19 cells. a A2E-laden ARPE-19 cells (A2E) were untransfected or transfected with a specific
    Figure Legend Snippet: Silencing p53 by transfection with specific oligonucleotide and siRNA protects ARPE-19 cells against cell death induced by blue light irradiation of A2E-laden ARPE-19 cells. a A2E-laden ARPE-19 cells (A2E) were untransfected or transfected with a specific

    Techniques Used: Transfection, Irradiation

    13) Product Images from "LonP1 Differently Modulates Mitochondrial Function and Bioenergetics of Primary Versus Metastatic Colon Cancer Cells"

    Article Title: LonP1 Differently Modulates Mitochondrial Function and Bioenergetics of Primary Versus Metastatic Colon Cancer Cells

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2018.00254

    LonP1 upregulation is associated with mutated p53 or nuclear β-ctn. (A) Representative immunohistochemical stainings of Ki-67, membrane β-ctn (m-βctn), nuclear β-ctn (n-βctn), and p53 in colorectal cancer (CRC) tissues. (B) Association between expression of LonP1, mutated p53, non-mutated p53, membrane β-ctn, or nuclear β-ctn in CRC tissues; * P
    Figure Legend Snippet: LonP1 upregulation is associated with mutated p53 or nuclear β-ctn. (A) Representative immunohistochemical stainings of Ki-67, membrane β-ctn (m-βctn), nuclear β-ctn (n-βctn), and p53 in colorectal cancer (CRC) tissues. (B) Association between expression of LonP1, mutated p53, non-mutated p53, membrane β-ctn, or nuclear β-ctn in CRC tissues; * P

    Techniques Used: Immunohistochemistry, Expressing

    14) Product Images from "Methylation of MGMT promoter does not predict response to temozolomide in patients with glioblastoma in Donostia Hospital"

    Article Title: Methylation of MGMT promoter does not predict response to temozolomide in patients with glioblastoma in Donostia Hospital

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-75477-9

    Representative images of Immunohistochemistry for molecular markers of glioblastoma. Images for Ki67 (high above and low below), p53 (positive staining above and negative below), and IDH1 (positive staining above and negative below) are presented.
    Figure Legend Snippet: Representative images of Immunohistochemistry for molecular markers of glioblastoma. Images for Ki67 (high above and low below), p53 (positive staining above and negative below), and IDH1 (positive staining above and negative below) are presented.

    Techniques Used: Immunohistochemistry, Staining

    Related Articles

    DNA Synthesis:

    Article Title: Inhibitory effect of PDGF-BB and serum-stimulated responses in vascular smooth muscle cell proliferation by hinokitiol via up-regulation of p21 and p53
    Article Snippet: The fold activity of LDH was calculated from the following equation: [(experimental LDH release)/(vehicle LDH release)]. .. VSMCs (2 × 105 cells/dish) were seeded in a 96-well microplate for 24 h and then serum-starved for 24 h. Following preincubation with hinokitiol for 20 min, the cells were treated with PDGF-BB (10 ng/ml) and 10% FBS serum for 48 h. DNA synthesis was assessed using BrdU incorporation assay kits (Roche Diagnostics, Rotkreuz, Switzerland) according to the manufacturer’s instructions. .. DNA synthesis in VSMCs was assessed by the incorporation of BrdU.

    BrdU Incorporation Assay:

    Article Title: Inhibitory effect of PDGF-BB and serum-stimulated responses in vascular smooth muscle cell proliferation by hinokitiol via up-regulation of p21 and p53
    Article Snippet: The fold activity of LDH was calculated from the following equation: [(experimental LDH release)/(vehicle LDH release)]. .. VSMCs (2 × 105 cells/dish) were seeded in a 96-well microplate for 24 h and then serum-starved for 24 h. Following preincubation with hinokitiol for 20 min, the cells were treated with PDGF-BB (10 ng/ml) and 10% FBS serum for 48 h. DNA synthesis was assessed using BrdU incorporation assay kits (Roche Diagnostics, Rotkreuz, Switzerland) according to the manufacturer’s instructions. .. DNA synthesis in VSMCs was assessed by the incorporation of BrdU.

    other:

    Article Title: Pre-clinical evaluation of the MDM2-p53 antagonist RG7388 alone and in combination with chemotherapy in neuroblastoma
    Article Snippet: In the isogenic Tet21N system, Tet21N MYCN+ cells were significantly more sensitive to RG7388 compared with Tet21N MYCN− cells (P < 0.005, paired t test, Figure ).

    Binding Assay:

    Article Title: Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway
    Article Snippet: Cell cycle distributions were assessed based on DNA contents by FACS using a Flow Cytometer (BD Biosciences, NJ). .. For apoptosis analysis, the indicated cells were harvested, washed with PBS, suspended in binding buffer, and sequentially stained with Annexin V-FITC Detection Kit (Roche Applied Science, Penzberg, Germany) by flow cytometer according to the manufacturer's protocol. .. Cell migration and invasion assays were assessed by transwell chambers (8.0 μm pore size; Millipore, MA) pre-coated with rat tail tendon collagen type 1 (0.5 mg/mL) on the lower surface.

    Staining:

    Article Title: Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway
    Article Snippet: Cell cycle distributions were assessed based on DNA contents by FACS using a Flow Cytometer (BD Biosciences, NJ). .. For apoptosis analysis, the indicated cells were harvested, washed with PBS, suspended in binding buffer, and sequentially stained with Annexin V-FITC Detection Kit (Roche Applied Science, Penzberg, Germany) by flow cytometer according to the manufacturer's protocol. .. Cell migration and invasion assays were assessed by transwell chambers (8.0 μm pore size; Millipore, MA) pre-coated with rat tail tendon collagen type 1 (0.5 mg/mL) on the lower surface.

    Flow Cytometry:

    Article Title: Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway
    Article Snippet: Cell cycle distributions were assessed based on DNA contents by FACS using a Flow Cytometer (BD Biosciences, NJ). .. For apoptosis analysis, the indicated cells were harvested, washed with PBS, suspended in binding buffer, and sequentially stained with Annexin V-FITC Detection Kit (Roche Applied Science, Penzberg, Germany) by flow cytometer according to the manufacturer's protocol. .. Cell migration and invasion assays were assessed by transwell chambers (8.0 μm pore size; Millipore, MA) pre-coated with rat tail tendon collagen type 1 (0.5 mg/mL) on the lower surface.

    Cytometry:

    Article Title: Epithelial cell-derived periostin functions as a tumor suppressor in gastric cancer through stabilizing p53 and E-cadherin proteins via the Rb/E2F1/p14ARF/Mdm2 signaling pathway
    Article Snippet: Cell cycle distributions were assessed based on DNA contents by FACS using a Flow Cytometer (BD Biosciences, NJ). .. For apoptosis analysis, the indicated cells were harvested, washed with PBS, suspended in binding buffer, and sequentially stained with Annexin V-FITC Detection Kit (Roche Applied Science, Penzberg, Germany) by flow cytometer according to the manufacturer's protocol. .. Cell migration and invasion assays were assessed by transwell chambers (8.0 μm pore size; Millipore, MA) pre-coated with rat tail tendon collagen type 1 (0.5 mg/mL) on the lower surface.

    Transfection:

    Article Title: A specific PP2A regulatory subunit, B56?, mediates DNA damage-induced dephosphorylation of p53 at Thr55
    Article Snippet: Cell cycle phase distributions of GFP-positive cells were determined by FACScan flow cytometry. .. To generate proliferation curves for HCT116 cells, cells were transfected with either B56γ3 or a control CMV empty vector using Fugene (Roche), seeded in triplicate and counted at 0, 24, 48, 72, 96 and 120 h post seeding. .. To generate proliferation curves for H1299 cells, cells were cotransfected with wild-type p53 or T55D and B56γ3 or a control CMV empty vector, seeded in triplicate and counted at 0, 24, 48, 72, 96 and 120 h post seeding.

    Article Title: The RNA helicase p68 modulates expression and function of the ?133 isoform(s) of p53, and is inversely associated with ?133p53 expression in breast cancer
    Article Snippet: siRNA transfections siRNA reverse transfections were performed using Lipofectamine™ RNAiMax (Invitrogen) and siRNA oligonucleotides (30pmols of p68 and 100pmols of TAp53- Dharmacon) ( ). .. Luciferase reporter assays H1299 cells were transfected using Fugene® 6 (Roche) with plasmids encoding p68, Δ133p53 and full-length p53, all under control of a CMV promoter, and appropriate promoters/luciferase reporters. .. A Renilla -luciferase control plasmid was co-transfected as a control for transfection efficiency.

    Plasmid Preparation:

    Article Title: A specific PP2A regulatory subunit, B56?, mediates DNA damage-induced dephosphorylation of p53 at Thr55
    Article Snippet: Cell cycle phase distributions of GFP-positive cells were determined by FACScan flow cytometry. .. To generate proliferation curves for HCT116 cells, cells were transfected with either B56γ3 or a control CMV empty vector using Fugene (Roche), seeded in triplicate and counted at 0, 24, 48, 72, 96 and 120 h post seeding. .. To generate proliferation curves for H1299 cells, cells were cotransfected with wild-type p53 or T55D and B56γ3 or a control CMV empty vector, seeded in triplicate and counted at 0, 24, 48, 72, 96 and 120 h post seeding.

    Article Title: p53 Represses Cyclin D1 Transcription through Down Regulation of Bcl-3 and Inducing Increased Association of the p52 NF-?B Subunit with Histone Deacetylase 1
    Article Snippet: .. The p52 expression plasmid (amino acids 1 to 405) and C-terminal p100 (amino acids 450 to 946) used in this report were generated by PCR by using the Pwo polymerase (Roche) and were subcloned into the same RSV expression plasmid backbone. .. Cyclin D1 and cyclin E promoter luciferase plasmids were obtained from Richard Pestell (Albert Einstein Cancer Center, Bronx, N.Y.).

    Luciferase:

    Article Title: The RNA helicase p68 modulates expression and function of the ?133 isoform(s) of p53, and is inversely associated with ?133p53 expression in breast cancer
    Article Snippet: siRNA transfections siRNA reverse transfections were performed using Lipofectamine™ RNAiMax (Invitrogen) and siRNA oligonucleotides (30pmols of p68 and 100pmols of TAp53- Dharmacon) ( ). .. Luciferase reporter assays H1299 cells were transfected using Fugene® 6 (Roche) with plasmids encoding p68, Δ133p53 and full-length p53, all under control of a CMV promoter, and appropriate promoters/luciferase reporters. .. A Renilla -luciferase control plasmid was co-transfected as a control for transfection efficiency.

    Expressing:

    Article Title: p53 Represses Cyclin D1 Transcription through Down Regulation of Bcl-3 and Inducing Increased Association of the p52 NF-?B Subunit with Histone Deacetylase 1
    Article Snippet: .. The p52 expression plasmid (amino acids 1 to 405) and C-terminal p100 (amino acids 450 to 946) used in this report were generated by PCR by using the Pwo polymerase (Roche) and were subcloned into the same RSV expression plasmid backbone. .. Cyclin D1 and cyclin E promoter luciferase plasmids were obtained from Richard Pestell (Albert Einstein Cancer Center, Bronx, N.Y.).

    Generated:

    Article Title: p53 Represses Cyclin D1 Transcription through Down Regulation of Bcl-3 and Inducing Increased Association of the p52 NF-?B Subunit with Histone Deacetylase 1
    Article Snippet: .. The p52 expression plasmid (amino acids 1 to 405) and C-terminal p100 (amino acids 450 to 946) used in this report were generated by PCR by using the Pwo polymerase (Roche) and were subcloned into the same RSV expression plasmid backbone. .. Cyclin D1 and cyclin E promoter luciferase plasmids were obtained from Richard Pestell (Albert Einstein Cancer Center, Bronx, N.Y.).

    Article Title: Loss of p53-inducible long non-coding RNA LINC01021 increases chemosensitivity
    Article Snippet: For conditional expression of p53 and LINC01021 from pRTR vectors, doxycycline (Sigma) was used at a final concentration of 100 ng/ml. .. RNA isolation and qPCR analysis Total RNA was prepared with the High Pure RNA Isolation Kit (Roche) according to the manufacturer´s protocol. cDNA was generated from 1 μg of total RNA per sample using anchored oligo(dT) primers (Verso cDNA Kit, Thermo Scientific). qPCR was performed by using the LightCycler 480 (Roche) and the Fast SYBR Green Master Mix (Applied Biosystems). ..

    Polymerase Chain Reaction:

    Article Title: p53 Represses Cyclin D1 Transcription through Down Regulation of Bcl-3 and Inducing Increased Association of the p52 NF-?B Subunit with Histone Deacetylase 1
    Article Snippet: .. The p52 expression plasmid (amino acids 1 to 405) and C-terminal p100 (amino acids 450 to 946) used in this report were generated by PCR by using the Pwo polymerase (Roche) and were subcloned into the same RSV expression plasmid backbone. .. Cyclin D1 and cyclin E promoter luciferase plasmids were obtained from Richard Pestell (Albert Einstein Cancer Center, Bronx, N.Y.).

    Isolation:

    Article Title: Loss of p53-inducible long non-coding RNA LINC01021 increases chemosensitivity
    Article Snippet: For conditional expression of p53 and LINC01021 from pRTR vectors, doxycycline (Sigma) was used at a final concentration of 100 ng/ml. .. RNA isolation and qPCR analysis Total RNA was prepared with the High Pure RNA Isolation Kit (Roche) according to the manufacturer´s protocol. cDNA was generated from 1 μg of total RNA per sample using anchored oligo(dT) primers (Verso cDNA Kit, Thermo Scientific). qPCR was performed by using the LightCycler 480 (Roche) and the Fast SYBR Green Master Mix (Applied Biosystems). ..

    Real-time Polymerase Chain Reaction:

    Article Title: Loss of p53-inducible long non-coding RNA LINC01021 increases chemosensitivity
    Article Snippet: For conditional expression of p53 and LINC01021 from pRTR vectors, doxycycline (Sigma) was used at a final concentration of 100 ng/ml. .. RNA isolation and qPCR analysis Total RNA was prepared with the High Pure RNA Isolation Kit (Roche) according to the manufacturer´s protocol. cDNA was generated from 1 μg of total RNA per sample using anchored oligo(dT) primers (Verso cDNA Kit, Thermo Scientific). qPCR was performed by using the LightCycler 480 (Roche) and the Fast SYBR Green Master Mix (Applied Biosystems). ..

    SYBR Green Assay:

    Article Title: Loss of p53-inducible long non-coding RNA LINC01021 increases chemosensitivity
    Article Snippet: For conditional expression of p53 and LINC01021 from pRTR vectors, doxycycline (Sigma) was used at a final concentration of 100 ng/ml. .. RNA isolation and qPCR analysis Total RNA was prepared with the High Pure RNA Isolation Kit (Roche) according to the manufacturer´s protocol. cDNA was generated from 1 μg of total RNA per sample using anchored oligo(dT) primers (Verso cDNA Kit, Thermo Scientific). qPCR was performed by using the LightCycler 480 (Roche) and the Fast SYBR Green Master Mix (Applied Biosystems). ..

    Lysis:

    Article Title: Mechanisms of G2 Arrest in Response to Overexpression of p53
    Article Snippet: Immune complexes were isolated with protein A– conjugated sepharose (Pharmacia, Bridgewater, NJ). .. Sepharose pellets were washed with lysis buffer and incubated for 30 min at 37°C in 20 mM HEPES, pH 7.9, 5 mM MgCl2 , 1 μg of histone H1 (Hoffman La Roche), 1 mM DTT, 100 μM unlabeled ATP, and 10 μCi of [γ-32 P]ATP in a total volume of 20 μl. .. Phosphorylated histone was separated by SDS-PAGE (12.5% acrylamide), and the dried gels were exposed to film.

    Incubation:

    Article Title: Mechanisms of G2 Arrest in Response to Overexpression of p53
    Article Snippet: Immune complexes were isolated with protein A– conjugated sepharose (Pharmacia, Bridgewater, NJ). .. Sepharose pellets were washed with lysis buffer and incubated for 30 min at 37°C in 20 mM HEPES, pH 7.9, 5 mM MgCl2 , 1 μg of histone H1 (Hoffman La Roche), 1 mM DTT, 100 μM unlabeled ATP, and 10 μCi of [γ-32 P]ATP in a total volume of 20 μl. .. Phosphorylated histone was separated by SDS-PAGE (12.5% acrylamide), and the dried gels were exposed to film.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Roche p53 mdm2 interaction
    Nutlin-3 treatment induces <t>p53</t> target gene expression in p53 wild-type laryngeal squamous cell carcinoma cells. Western blot analysis of laryngeal squamous cell carcinoma cells harvested 48 h after either no treatment, treatment with DMSO (vehicle control) or treatment with Nutlin-3 at 0.5 μ or 5.0 μ as indicated. All lanes were loaded with 50 μ g of protein. Blots were probed with antibodies for p53, <t>MDM2,</t> p21 and β -actin (protein loading control) as indicated. Note the absence of any detectable p53 in UM-SCC-12 cells, known to be p53 null from DNA sequence analysis (Q104Stop, LOH). UM-SCC-5 shows two distinct bands of p53 protein, indicative of a well-documented polymorphism in codon 72, which was also confirmed by DNA sequence analysis (codon 72 is Pro/Arg, data not shown). The results shown are from a typical experiment repeated on at least three occasions.
    P53 Mdm2 Interaction, supplied by Roche, 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/p53 mdm2 interaction/product/Roche
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p53 mdm2 interaction - by Bioz Stars, 2021-06
    86/100 stars
      Buy from Supplier

    86
    Roche p53 pan elisa kit
    Expression of <t>p53</t> and p21/WAF1 tested by <t>ELISA</t> in A549cells. A549 cells were incubated with or without TV (15 μM) for 3, 6, 12, 24, and 48 h. (A) The level of p53 in A549 cells, (B) the amount of p21/WAF1 in A549 cells. Each value is the mean ± S.D. of three independent experiments. *p
    P53 Pan Elisa Kit, supplied by Roche, 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/p53 pan elisa kit/product/Roche
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p53 pan elisa kit - by Bioz Stars, 2021-06
    86/100 stars
      Buy from Supplier

    86
    Roche tp53 flag cdna
    Generation of <t>DanG-TREx-TP53</t> and MiaPaCa-2-TREx-TP53 cells with Dox-inducible expression of functionally active wt TP53. ( A ) The plasmids pcDNA6/TR and pcDNA4/TO-TP53FLAG were sequentially transfected into DanG and MiaPaCa-2 cells bearing mutant endogenous p53 and clones with inducible expression of wt TP53 were selected (DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53). Cells were cultured for 96 h in the presence or absence of Dox and lysates were prepared for western blot analysis of <t>FLAG</t> (upper panel) and TP53 (second panel) at the indicated time points. Equal amounts of protein (10 μ g) were separated on SDS polyacrylamide gel electrophoresis (PAGE). Furthermore, effects of Dox-induced wt TP53 expression on downstream targets were investigated by western blot analysis: p21 WAF1/CIP1 , cyclin-dependent kinase-2, cyclin A and β -actin (lower panels). Equal amounts of protein (30 μ g) were separated on SDS–PAGE. ( B ) Effects on cell cycle after wt TP53 expression in DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 were analysed by FACS over a time course of 96 h. At every 24 h, cells were fixed with 70% ethanol and stained with propidium iodide. ( C ) Time-dependent proliferation of DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 cells in the presence or absence of Dox as determined by alamar blue assay. At every 24 h, alamar blue dye was applied to the media of cells and fluorescence was determined as an indirect measurement of cell numbers. ( D ) Immunoblot demonstrating expression of poly(ADP-ribose)polymerase (p116) and/or its apoptosis-related cleavage product p85 in untreated controls and cells that had been treated with Dox, IFN- γ or a combination of both for 72 or 96 h. Whole-cell lysates were separated by 7.5% SDS–PAGE. ( E ) The diagram depicts the concentration dependence of the growth inhibition by gemcitabine with data presented as a percentage of the respective controls (vehicle and +Dox, respectively). ( F ) The response of the MiaPaCa-2-TREx-TP53 cells to gemcitabine was evaluated by determination of cell numbers. The cells were treated with −/+Dox and −/+gemcitabine, as indicated, for 48 h. The diagram presents cell numbers after treatment with or without 10 μ g ml −1 gemcitabine. ( G ) Cellular senescence ( β -Gal activity) in MiaPaCa-2-TREx-TP53 cells was detected by a cell senescence assay after −/+Dox treatment. Senescence-positive cells appeared blue ( × 200 magnification). A representative experiment out of two is shown.
    Tp53 Flag Cdna, supplied by Roche, 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/tp53 flag cdna/product/Roche
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tp53 flag cdna - by Bioz Stars, 2021-06
    86/100 stars
      Buy from Supplier

    86
    Roche tp53 mutations
    Allele frequencies of <t>TP53</t> mutations in different cell types The allele frequencies of TP53 mutations were determined in CD34+ and CD34– cells isolated from bone marrow and CD14+ monocytes, CD3+ T lymphocytes and granulocytes isolated from peripheral blood of lower-risk MDS patients. Each column represents variant allele frequency (VAF) of TP53 mutations in particular cell type of individual patient.
    Tp53 Mutations, supplied by Roche, 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/tp53 mutations/product/Roche
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tp53 mutations - by Bioz Stars, 2021-06
    86/100 stars
      Buy from Supplier

    Image Search Results


    Nutlin-3 treatment induces p53 target gene expression in p53 wild-type laryngeal squamous cell carcinoma cells. Western blot analysis of laryngeal squamous cell carcinoma cells harvested 48 h after either no treatment, treatment with DMSO (vehicle control) or treatment with Nutlin-3 at 0.5 μ or 5.0 μ as indicated. All lanes were loaded with 50 μ g of protein. Blots were probed with antibodies for p53, MDM2, p21 and β -actin (protein loading control) as indicated. Note the absence of any detectable p53 in UM-SCC-12 cells, known to be p53 null from DNA sequence analysis (Q104Stop, LOH). UM-SCC-5 shows two distinct bands of p53 protein, indicative of a well-documented polymorphism in codon 72, which was also confirmed by DNA sequence analysis (codon 72 is Pro/Arg, data not shown). The results shown are from a typical experiment repeated on at least three occasions.

    Journal: British Journal of Cancer

    Article Title: Nutlin-3, the small-molecule inhibitor of MDM2, promotes senescence and radiosensitises laryngeal carcinoma cells harbouring wild-type p53

    doi: 10.1038/sj.bjc.6605739

    Figure Lengend Snippet: Nutlin-3 treatment induces p53 target gene expression in p53 wild-type laryngeal squamous cell carcinoma cells. Western blot analysis of laryngeal squamous cell carcinoma cells harvested 48 h after either no treatment, treatment with DMSO (vehicle control) or treatment with Nutlin-3 at 0.5 μ or 5.0 μ as indicated. All lanes were loaded with 50 μ g of protein. Blots were probed with antibodies for p53, MDM2, p21 and β -actin (protein loading control) as indicated. Note the absence of any detectable p53 in UM-SCC-12 cells, known to be p53 null from DNA sequence analysis (Q104Stop, LOH). UM-SCC-5 shows two distinct bands of p53 protein, indicative of a well-documented polymorphism in codon 72, which was also confirmed by DNA sequence analysis (codon 72 is Pro/Arg, data not shown). The results shown are from a typical experiment repeated on at least three occasions.

    Article Snippet: One drug that targets the p53-binding pocket of MDM2 and thus acts to inhibit p53/MDM2 interaction is Nutlin-3, developed by Roche (Nutley, NJ, USA) ( ; ; ).

    Techniques: Expressing, Western Blot, Sequencing

    Expression of p53 and p21/WAF1 tested by ELISA in A549cells. A549 cells were incubated with or without TV (15 μM) for 3, 6, 12, 24, and 48 h. (A) The level of p53 in A549 cells, (B) the amount of p21/WAF1 in A549 cells. Each value is the mean ± S.D. of three independent experiments. *p

    Journal: Biomolecules & Therapeutics

    Article Title: Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells

    doi: 10.4062/biomolther.2012.20.2.177

    Figure Lengend Snippet: Expression of p53 and p21/WAF1 tested by ELISA in A549cells. A549 cells were incubated with or without TV (15 μM) for 3, 6, 12, 24, and 48 h. (A) The level of p53 in A549 cells, (B) the amount of p21/WAF1 in A549 cells. Each value is the mean ± S.D. of three independent experiments. *p

    Article Snippet: Except for those indicated intentionally, all the materials were purchased from commercial sources, including: MTT, DMSO, propidium iodide, RNase A, and trypan (Sigma Aldrich Chemical Co., St. Louis, MO); BD ApoAlertTM Caspase-3, -8 Colorimetric Assay Kits and ApoAlert Caspase9/6 Fluorescence Assay Kits (Clontech Laboratories, Inc., Palo Alto, CA); PBS, HEPES, DMEM (Dulbecco’s modified Eagle’s medium), fetal bovine serum, and culture media (Life Technologies, Inc., Grand Island, NY); Bromodeoxyuridine (BrdU) Cell Proliferation Assay Kit (Oncogene Research, Cambridge, MA); Lactate Dehydrogenase (LDH) Kit (ZhongSheng Co., Beijing, China); p53 pan ELISA Kit (Roche Diagnostics GmbH, Germany); WAF1 ELISA, Fas ligand and Fas ELISA Kits (Calbiochem, Cambridge, MA).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Incubation

    Generation of DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 cells with Dox-inducible expression of functionally active wt TP53. ( A ) The plasmids pcDNA6/TR and pcDNA4/TO-TP53FLAG were sequentially transfected into DanG and MiaPaCa-2 cells bearing mutant endogenous p53 and clones with inducible expression of wt TP53 were selected (DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53). Cells were cultured for 96 h in the presence or absence of Dox and lysates were prepared for western blot analysis of FLAG (upper panel) and TP53 (second panel) at the indicated time points. Equal amounts of protein (10 μ g) were separated on SDS polyacrylamide gel electrophoresis (PAGE). Furthermore, effects of Dox-induced wt TP53 expression on downstream targets were investigated by western blot analysis: p21 WAF1/CIP1 , cyclin-dependent kinase-2, cyclin A and β -actin (lower panels). Equal amounts of protein (30 μ g) were separated on SDS–PAGE. ( B ) Effects on cell cycle after wt TP53 expression in DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 were analysed by FACS over a time course of 96 h. At every 24 h, cells were fixed with 70% ethanol and stained with propidium iodide. ( C ) Time-dependent proliferation of DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 cells in the presence or absence of Dox as determined by alamar blue assay. At every 24 h, alamar blue dye was applied to the media of cells and fluorescence was determined as an indirect measurement of cell numbers. ( D ) Immunoblot demonstrating expression of poly(ADP-ribose)polymerase (p116) and/or its apoptosis-related cleavage product p85 in untreated controls and cells that had been treated with Dox, IFN- γ or a combination of both for 72 or 96 h. Whole-cell lysates were separated by 7.5% SDS–PAGE. ( E ) The diagram depicts the concentration dependence of the growth inhibition by gemcitabine with data presented as a percentage of the respective controls (vehicle and +Dox, respectively). ( F ) The response of the MiaPaCa-2-TREx-TP53 cells to gemcitabine was evaluated by determination of cell numbers. The cells were treated with −/+Dox and −/+gemcitabine, as indicated, for 48 h. The diagram presents cell numbers after treatment with or without 10 μ g ml −1 gemcitabine. ( G ) Cellular senescence ( β -Gal activity) in MiaPaCa-2-TREx-TP53 cells was detected by a cell senescence assay after −/+Dox treatment. Senescence-positive cells appeared blue ( × 200 magnification). A representative experiment out of two is shown.

    Journal: British Journal of Cancer

    Article Title: The proline TP53 variant stimulates likely lymphangiogenesis in an orthotopic mouse model of pancreatic cancer

    doi: 10.1038/bjc.2011.521

    Figure Lengend Snippet: Generation of DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 cells with Dox-inducible expression of functionally active wt TP53. ( A ) The plasmids pcDNA6/TR and pcDNA4/TO-TP53FLAG were sequentially transfected into DanG and MiaPaCa-2 cells bearing mutant endogenous p53 and clones with inducible expression of wt TP53 were selected (DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53). Cells were cultured for 96 h in the presence or absence of Dox and lysates were prepared for western blot analysis of FLAG (upper panel) and TP53 (second panel) at the indicated time points. Equal amounts of protein (10 μ g) were separated on SDS polyacrylamide gel electrophoresis (PAGE). Furthermore, effects of Dox-induced wt TP53 expression on downstream targets were investigated by western blot analysis: p21 WAF1/CIP1 , cyclin-dependent kinase-2, cyclin A and β -actin (lower panels). Equal amounts of protein (30 μ g) were separated on SDS–PAGE. ( B ) Effects on cell cycle after wt TP53 expression in DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 were analysed by FACS over a time course of 96 h. At every 24 h, cells were fixed with 70% ethanol and stained with propidium iodide. ( C ) Time-dependent proliferation of DanG-TREx-TP53 and MiaPaCa-2-TREx-TP53 cells in the presence or absence of Dox as determined by alamar blue assay. At every 24 h, alamar blue dye was applied to the media of cells and fluorescence was determined as an indirect measurement of cell numbers. ( D ) Immunoblot demonstrating expression of poly(ADP-ribose)polymerase (p116) and/or its apoptosis-related cleavage product p85 in untreated controls and cells that had been treated with Dox, IFN- γ or a combination of both for 72 or 96 h. Whole-cell lysates were separated by 7.5% SDS–PAGE. ( E ) The diagram depicts the concentration dependence of the growth inhibition by gemcitabine with data presented as a percentage of the respective controls (vehicle and +Dox, respectively). ( F ) The response of the MiaPaCa-2-TREx-TP53 cells to gemcitabine was evaluated by determination of cell numbers. The cells were treated with −/+Dox and −/+gemcitabine, as indicated, for 48 h. The diagram presents cell numbers after treatment with or without 10 μ g ml −1 gemcitabine. ( G ) Cellular senescence ( β -Gal activity) in MiaPaCa-2-TREx-TP53 cells was detected by a cell senescence assay after −/+Dox treatment. Senescence-positive cells appeared blue ( × 200 magnification). A representative experiment out of two is shown.

    Article Snippet: The TP53-FLAG cDNA was restricted by endonuclease Not I (Roche), inserted in pcDNA4/TO and identified by restriction with endonuclease Pvu II (Roche).

    Techniques: Expressing, Transfection, Mutagenesis, Clone Assay, Cell Culture, Western Blot, Polyacrylamide Gel Electrophoresis, SDS Page, FACS, Staining, Alamar Blue Assay, Fluorescence, Concentration Assay, Inhibition, Activity Assay

    Induction of wt TP53 expression reduced primary tumour growth in orthotopic MiaPaCa-2 pancreatic carcinomas at both time points. MiaPaCa-2-TREx-TP53 cells were grown orthotopically in the pancreas of mice treated with or without Dox as indicated. At the end of treatment (either 4 weeks or 8 weeks) tumour weights were determined. ( A ) Open situs of representative mice from each control (−Dox) and treatment group (+Dox). ( B ) Conformation of wt TP53 induction in vivo . Primary tumours were analysed for TP53 expression by immunohistochemistry using an antibody against the FLAG-tag. Examples of wt TP53 expression at 4 and 8 weeks of tumour growth, with detection of the wt TP53-FLAG protein in the nucleus of tumour cells from Dox-treated mice indicated by the light blue arrows. In contrast, no signal was obtained in control tumours (−Dox) (images at × 200 magnification). ( C ) Summary of primary tumour weights of Dox-treated or -untreated animals receiving Dox either in weeks 1–4 or in weeks 5–8. Data represent mean±s.e.m. for each group. * P

    Journal: British Journal of Cancer

    Article Title: The proline TP53 variant stimulates likely lymphangiogenesis in an orthotopic mouse model of pancreatic cancer

    doi: 10.1038/bjc.2011.521

    Figure Lengend Snippet: Induction of wt TP53 expression reduced primary tumour growth in orthotopic MiaPaCa-2 pancreatic carcinomas at both time points. MiaPaCa-2-TREx-TP53 cells were grown orthotopically in the pancreas of mice treated with or without Dox as indicated. At the end of treatment (either 4 weeks or 8 weeks) tumour weights were determined. ( A ) Open situs of representative mice from each control (−Dox) and treatment group (+Dox). ( B ) Conformation of wt TP53 induction in vivo . Primary tumours were analysed for TP53 expression by immunohistochemistry using an antibody against the FLAG-tag. Examples of wt TP53 expression at 4 and 8 weeks of tumour growth, with detection of the wt TP53-FLAG protein in the nucleus of tumour cells from Dox-treated mice indicated by the light blue arrows. In contrast, no signal was obtained in control tumours (−Dox) (images at × 200 magnification). ( C ) Summary of primary tumour weights of Dox-treated or -untreated animals receiving Dox either in weeks 1–4 or in weeks 5–8. Data represent mean±s.e.m. for each group. * P

    Article Snippet: The TP53-FLAG cDNA was restricted by endonuclease Not I (Roche), inserted in pcDNA4/TO and identified by restriction with endonuclease Pvu II (Roche).

    Techniques: Expressing, Mouse Assay, In Vivo, Immunohistochemistry, FLAG-tag

    Allele frequencies of TP53 mutations in different cell types The allele frequencies of TP53 mutations were determined in CD34+ and CD34– cells isolated from bone marrow and CD14+ monocytes, CD3+ T lymphocytes and granulocytes isolated from peripheral blood of lower-risk MDS patients. Each column represents variant allele frequency (VAF) of TP53 mutations in particular cell type of individual patient.

    Journal: Oncotarget

    Article Title: TP53 mutation variant allele frequency is a potential predictor for clinical outcome of patients with lower-risk myelodysplastic syndromes

    doi: 10.18632/oncotarget.9200

    Figure Lengend Snippet: Allele frequencies of TP53 mutations in different cell types The allele frequencies of TP53 mutations were determined in CD34+ and CD34– cells isolated from bone marrow and CD14+ monocytes, CD3+ T lymphocytes and granulocytes isolated from peripheral blood of lower-risk MDS patients. Each column represents variant allele frequency (VAF) of TP53 mutations in particular cell type of individual patient.

    Article Snippet: TP53 mutations may initiate malignant transformation in lower-risk MDS, induce the more aggressive growth of clones, or provide survival advantages for mutated cells, such as increased proliferation or reduced apoptosis in more advanced stages of MDS.

    Techniques: Isolation, Variant Assay

    Distribution of TP53 somatic mutations in lower-risk MDS patients ( A ) Frequency of TP53 mutations in lower-risk MDS patients with and without del(5q). ( B ) Pie chart representing the different TP53 mutation types detected in entire patient cohort.

    Journal: Oncotarget

    Article Title: TP53 mutation variant allele frequency is a potential predictor for clinical outcome of patients with lower-risk myelodysplastic syndromes

    doi: 10.18632/oncotarget.9200

    Figure Lengend Snippet: Distribution of TP53 somatic mutations in lower-risk MDS patients ( A ) Frequency of TP53 mutations in lower-risk MDS patients with and without del(5q). ( B ) Pie chart representing the different TP53 mutation types detected in entire patient cohort.

    Article Snippet: TP53 mutations may initiate malignant transformation in lower-risk MDS, induce the more aggressive growth of clones, or provide survival advantages for mutated cells, such as increased proliferation or reduced apoptosis in more advanced stages of MDS.

    Techniques: Mutagenesis

    Kaplan–Meier curves of overall survival (OS) and progression-free survival (PFS) according to TP53 mutational status and mutational burden ( A , C ) Comparison of OS and PFS between patients with TP53 mutations and those with wild-type TP53. ( B , D ) Comparison of OS and PFS between patients stratified by the mutational burden and the time of mutation appearance into four groups (the first group: patients with wild-type TP53 ; the second group: patients with > 6% VAF of TP53 mutations at the time of diagnosis; the third group: patients with

    Journal: Oncotarget

    Article Title: TP53 mutation variant allele frequency is a potential predictor for clinical outcome of patients with lower-risk myelodysplastic syndromes

    doi: 10.18632/oncotarget.9200

    Figure Lengend Snippet: Kaplan–Meier curves of overall survival (OS) and progression-free survival (PFS) according to TP53 mutational status and mutational burden ( A , C ) Comparison of OS and PFS between patients with TP53 mutations and those with wild-type TP53. ( B , D ) Comparison of OS and PFS between patients stratified by the mutational burden and the time of mutation appearance into four groups (the first group: patients with wild-type TP53 ; the second group: patients with > 6% VAF of TP53 mutations at the time of diagnosis; the third group: patients with

    Article Snippet: TP53 mutations may initiate malignant transformation in lower-risk MDS, induce the more aggressive growth of clones, or provide survival advantages for mutated cells, such as increased proliferation or reduced apoptosis in more advanced stages of MDS.

    Techniques: Mutagenesis

    Time course of the TP53 mutant allele burden in serial follow-up samples of lower-risk MDS The frequency of TP53 mutations during follow-up of individual patients stratified by the mutational burden and the time of mutation acquisition. ( A ) The first group of patients with VAF > 6% at the time of diagnosis; ( B ) the second group with VAF

    Journal: Oncotarget

    Article Title: TP53 mutation variant allele frequency is a potential predictor for clinical outcome of patients with lower-risk myelodysplastic syndromes

    doi: 10.18632/oncotarget.9200

    Figure Lengend Snippet: Time course of the TP53 mutant allele burden in serial follow-up samples of lower-risk MDS The frequency of TP53 mutations during follow-up of individual patients stratified by the mutational burden and the time of mutation acquisition. ( A ) The first group of patients with VAF > 6% at the time of diagnosis; ( B ) the second group with VAF

    Article Snippet: TP53 mutations may initiate malignant transformation in lower-risk MDS, induce the more aggressive growth of clones, or provide survival advantages for mutated cells, such as increased proliferation or reduced apoptosis in more advanced stages of MDS.

    Techniques: Mutagenesis