human p53  (OriGene)


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  • 93
    Name:
    p53 TP53 NM 000546 Human Untagged Clone
    Description:
    TP53 untagged Human tumor protein p53 TP53 transcript variant 1
    Catalog Number:
    SC119832
    Price:
    560.0
    Category:
    Expression Plasmids
    Size:
    10 µg
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    Structured Review

    OriGene human p53
    Abhd5 Deficiency Induces EMT via inactivating <t>p53</t>
    TP53 untagged Human tumor protein p53 TP53 transcript variant 1
    https://www.bioz.com/result/human p53/product/OriGene
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human p53 - by Bioz Stars, 2021-06
    93/100 stars

    Images

    1) Product Images from "Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition"

    Article Title: Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition

    Journal: Cell reports

    doi: 10.1016/j.celrep.2014.11.016

    Abhd5 Deficiency Induces EMT via inactivating p53
    Figure Legend Snippet: Abhd5 Deficiency Induces EMT via inactivating p53

    Techniques Used:

    Aerobic Glycolysis Induces p53 Suppression via Inactivating AMPK in Abhd5-deficient Cells
    Figure Legend Snippet: Aerobic Glycolysis Induces p53 Suppression via Inactivating AMPK in Abhd5-deficient Cells

    Techniques Used:

    2) Product Images from "Zinc deficiency causes neural tube defects through attenuation of p53 ubiquitylation"

    Article Title: Zinc deficiency causes neural tube defects through attenuation of p53 ubiquitylation

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.169797

    Inhibition of p53 transactivation function overcomes zinc deficiency-induced failure of neural tube closure. (A) Still frames from time-lapse live imaging of E8.5 Ven Myr embryos show that an inhibitor of p53 transactivation function, pifithrin-α, but not an inhibitor of p53 mitochondrial function, pifithrin-µ, can rescue TPEN-induced failure of neural tube closure. (B) Time to neural tube closure after TPEN+pifithrin-α ( n =6 from three independent experiments) relative to control ( n =6 from four independent experiments) (the neural tube never closes with TPEN treatment) ( n =6 from two independent experiments) or TPEN +pifithrin-µ-treated embryos ( n =5 from two independent experiments). (C-F) Representative still images (C) and quantitative data (D-F) of time-lapse imaging show the ability of pifithrin-α to rescue TPEN-induced failure of neural tube closure. In A and C, the white lines, red lines, yellow lines and purple line show the edges of neural fold. In D, the pink arrowhead indicates failure of neural tube closure; the dark gray and green arrowheads indicate the timepoint of neural tube closure. * P
    Figure Legend Snippet: Inhibition of p53 transactivation function overcomes zinc deficiency-induced failure of neural tube closure. (A) Still frames from time-lapse live imaging of E8.5 Ven Myr embryos show that an inhibitor of p53 transactivation function, pifithrin-α, but not an inhibitor of p53 mitochondrial function, pifithrin-µ, can rescue TPEN-induced failure of neural tube closure. (B) Time to neural tube closure after TPEN+pifithrin-α ( n =6 from three independent experiments) relative to control ( n =6 from four independent experiments) (the neural tube never closes with TPEN treatment) ( n =6 from two independent experiments) or TPEN +pifithrin-µ-treated embryos ( n =5 from two independent experiments). (C-F) Representative still images (C) and quantitative data (D-F) of time-lapse imaging show the ability of pifithrin-α to rescue TPEN-induced failure of neural tube closure. In A and C, the white lines, red lines, yellow lines and purple line show the edges of neural fold. In D, the pink arrowhead indicates failure of neural tube closure; the dark gray and green arrowheads indicate the timepoint of neural tube closure. * P

    Techniques Used: Inhibition, Imaging

    Model for the proposed mechanism of zinc deficiency-induced failure of neural tube closure. In the presence of zinc, Mdm2 protein can bind and ubiquitylate p53, resulting in p53 degradation, maintenance of cell survival and proper neural tube closure. Zinc deficiency attenuates Mdm2 binding and activity toward p53, resulting in p53 stabilization and an increase in p53 transcriptional activity, causing cell death and failure of neural tube closure.
    Figure Legend Snippet: Model for the proposed mechanism of zinc deficiency-induced failure of neural tube closure. In the presence of zinc, Mdm2 protein can bind and ubiquitylate p53, resulting in p53 degradation, maintenance of cell survival and proper neural tube closure. Zinc deficiency attenuates Mdm2 binding and activity toward p53, resulting in p53 stabilization and an increase in p53 transcriptional activity, causing cell death and failure of neural tube closure.

    Techniques Used: Binding Assay, Activity Assay

    Zinc deficiency attenuates p53 ubiquitylation. (A) Schematic of the regulation of p53 ubiquitylation by the zinc-regulated E3 ubiquitin ligase Mdm2 and by the p53-deubiquitylating enzyme Hausp, leading to p53 degradation or stabilization. The N terminus of Mdm2 binds p53 via a TAZ domain, whereas the C-terminal zinc-regulated RING domain is required for ubiquitin ligase activity towards p53. TAZ, transactive zone. (B) E9.5 primary neuroepithelial cells treated with MG132 proteasome inhibitor and TPEN or TPEN+ZnSO 4 , followed by p53 co-immunoprecipitation and western blot analysis with antibodies against ubiquitin and Hausp shows TPEN decreases p53 ubiquitylation and Hausp binding. Graph shows western blot quantification data. Immunoprecipitated p53 is used as a loading control. Data are mean±s.d. All treatments were normalized to control. * P
    Figure Legend Snippet: Zinc deficiency attenuates p53 ubiquitylation. (A) Schematic of the regulation of p53 ubiquitylation by the zinc-regulated E3 ubiquitin ligase Mdm2 and by the p53-deubiquitylating enzyme Hausp, leading to p53 degradation or stabilization. The N terminus of Mdm2 binds p53 via a TAZ domain, whereas the C-terminal zinc-regulated RING domain is required for ubiquitin ligase activity towards p53. TAZ, transactive zone. (B) E9.5 primary neuroepithelial cells treated with MG132 proteasome inhibitor and TPEN or TPEN+ZnSO 4 , followed by p53 co-immunoprecipitation and western blot analysis with antibodies against ubiquitin and Hausp shows TPEN decreases p53 ubiquitylation and Hausp binding. Graph shows western blot quantification data. Immunoprecipitated p53 is used as a loading control. Data are mean±s.d. All treatments were normalized to control. * P

    Techniques Used: Activity Assay, Immunoprecipitation, Western Blot, Binding Assay

    p53 plays a crucial role in zinc deficiency-induced apoptosis. Western blot analysis of brain tissue from E9.5 embryos (each sample was pooled from four or five embryos, three independent experiments were performed) (A) and E9.5 primary neuroepithelial cells (from three independent experiments) (B) demonstrate that p53 levels increased in both the cytoplasm and nucleus after TPEN treatment for the indicated length of time, and p53 levels in both cellular compartments were reduced by concurrent zinc supplementation. Graphs show the corresponding quantification results of western blots. Data are mean±s.d. * P
    Figure Legend Snippet: p53 plays a crucial role in zinc deficiency-induced apoptosis. Western blot analysis of brain tissue from E9.5 embryos (each sample was pooled from four or five embryos, three independent experiments were performed) (A) and E9.5 primary neuroepithelial cells (from three independent experiments) (B) demonstrate that p53 levels increased in both the cytoplasm and nucleus after TPEN treatment for the indicated length of time, and p53 levels in both cellular compartments were reduced by concurrent zinc supplementation. Graphs show the corresponding quantification results of western blots. Data are mean±s.d. * P

    Techniques Used: Western Blot

    Related Articles

    Expressing:

    Article Title: Molecular mechanism leading to SAHA-induced autophagy in tumor cells: evidence for a p53-dependent pathway
    Article Snippet: Protein expression was quantified using Image J software. .. TP53 gene transfer The expression vector pCMV6-XL5 containing the human full-length cDNA for TP53 (TP53-WT) (NCBI Acc.-No: NM_000546.2; SC119832) was obtained from OriGene (Rockville, CA, USA). .. Originating from TP53-WT, a control vector containing the 637C > T mutation was constructed (TP53-637C > T) by using the QuikChange II Site-Directed Mutagenesis Kit (Agilent Technologies; CA, USA).

    Article Title: Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition
    Article Snippet: Construction of constitutively active (CA) and dominant-negative (DN) α1 and α2 AMPK expression vectors was described previously ( ). .. The expression plasmid of human p53 (# SC119832) and the control empty vector pCMV6-XL5 were purchased from ORIGENE. .. Cell apoptosis was assessed by flow cytometry of Annexin V/PI (Sigma) staining.

    Article Title: CELF1/p53 axis: a sustained antiproliferative signal leading to villus atrophy under total parenteral nutrition.
    Article Snippet: .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood. .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood.

    Plasmid Preparation:

    Article Title: Molecular mechanism leading to SAHA-induced autophagy in tumor cells: evidence for a p53-dependent pathway
    Article Snippet: Protein expression was quantified using Image J software. .. TP53 gene transfer The expression vector pCMV6-XL5 containing the human full-length cDNA for TP53 (TP53-WT) (NCBI Acc.-No: NM_000546.2; SC119832) was obtained from OriGene (Rockville, CA, USA). .. Originating from TP53-WT, a control vector containing the 637C > T mutation was constructed (TP53-637C > T) by using the QuikChange II Site-Directed Mutagenesis Kit (Agilent Technologies; CA, USA).

    Article Title: Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition
    Article Snippet: Construction of constitutively active (CA) and dominant-negative (DN) α1 and α2 AMPK expression vectors was described previously ( ). .. The expression plasmid of human p53 (# SC119832) and the control empty vector pCMV6-XL5 were purchased from ORIGENE. .. Cell apoptosis was assessed by flow cytometry of Annexin V/PI (Sigma) staining.

    Article Title: CELF1/p53 axis: a sustained antiproliferative signal leading to villus atrophy under total parenteral nutrition.
    Article Snippet: .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood. .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood.

    Article Title: Erb-B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53-responsive microRNA-3184-5p in cervical cancer cells
    Article Snippet: For in vitro experiments, Mithramycin A dissolved in DMSO at concentrations of 0 (vehicle control), 50 and 100 nM was used to treat cells for 48 h at 37°C in a 5% CO2 incubator. .. Transfections SiHa cells were transfected with plasmid vectors, while HeLa cells were transfected with small-interfering RNAs (siRNAs). pCMV6-XL4/5 plasmid vectors containing the TrueClone® human cDNA sequences for human TP53 (NM_000546; cat. no. SC119832), PIK3CA (NM_006218; cat. no. SC116227) or ERBB2 (NM_004448; cat. no. SC128161), and an empty negative control (NC) plasmid vector (cat. no. PCMV6XL5) were obtained from OriGene Technologies, Inc. For plasmid transfections, cells were seeded in 6-well plates (1.5×105 cells/well) and transiently transfected with 1 µg plasmid using Lipofectamine® 3000 transfection reagent (Invitrogen; Thermo Fisher Scientific, Inc.) for 20 min at room temperature and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. siRNAs targeting human ERBB2 (ERBB2-siRNA; cat. no. sc-29405), human PIK3CA (PIK3CA-siRNA; cat. no. sc-39127) and scrambled control (scr-siRNA; cat. no. sc-37007) were obtained from Santa Cruz Biotechnology, Inc. For siRNA transfections, cells were seeded in 6-well plates (2×105 cells/well) and transiently transfected with 80 pmol siRNA using Lipofectamine 3000 transfection reagent for 7 h at 37°C and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. miR-3184-5p (miRBase accession no. MIMAT0015064) mirVana® miRNA mimic (cat. no. 4464066) and mirVana® miRNA inhibitor (cat. no. 4464084), as well as the corresponding controls (cat. nos. .. 4464058 and 4464078, respectively), were obtained from AmbionÒ (Thermo Fisher Scientific, Inc.).

    Transfection:

    Article Title: CELF1/p53 axis: a sustained antiproliferative signal leading to villus atrophy under total parenteral nutrition.
    Article Snippet: .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood. .. Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN).. Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood.

    Article Title: Erb-B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53-responsive microRNA-3184-5p in cervical cancer cells
    Article Snippet: For in vitro experiments, Mithramycin A dissolved in DMSO at concentrations of 0 (vehicle control), 50 and 100 nM was used to treat cells for 48 h at 37°C in a 5% CO2 incubator. .. Transfections SiHa cells were transfected with plasmid vectors, while HeLa cells were transfected with small-interfering RNAs (siRNAs). pCMV6-XL4/5 plasmid vectors containing the TrueClone® human cDNA sequences for human TP53 (NM_000546; cat. no. SC119832), PIK3CA (NM_006218; cat. no. SC116227) or ERBB2 (NM_004448; cat. no. SC128161), and an empty negative control (NC) plasmid vector (cat. no. PCMV6XL5) were obtained from OriGene Technologies, Inc. For plasmid transfections, cells were seeded in 6-well plates (1.5×105 cells/well) and transiently transfected with 1 µg plasmid using Lipofectamine® 3000 transfection reagent (Invitrogen; Thermo Fisher Scientific, Inc.) for 20 min at room temperature and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. siRNAs targeting human ERBB2 (ERBB2-siRNA; cat. no. sc-29405), human PIK3CA (PIK3CA-siRNA; cat. no. sc-39127) and scrambled control (scr-siRNA; cat. no. sc-37007) were obtained from Santa Cruz Biotechnology, Inc. For siRNA transfections, cells were seeded in 6-well plates (2×105 cells/well) and transiently transfected with 80 pmol siRNA using Lipofectamine 3000 transfection reagent for 7 h at 37°C and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. miR-3184-5p (miRBase accession no. MIMAT0015064) mirVana® miRNA mimic (cat. no. 4464066) and mirVana® miRNA inhibitor (cat. no. 4464084), as well as the corresponding controls (cat. nos. .. 4464058 and 4464078, respectively), were obtained from AmbionÒ (Thermo Fisher Scientific, Inc.).

    Negative Control:

    Article Title: Erb-B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53-responsive microRNA-3184-5p in cervical cancer cells
    Article Snippet: For in vitro experiments, Mithramycin A dissolved in DMSO at concentrations of 0 (vehicle control), 50 and 100 nM was used to treat cells for 48 h at 37°C in a 5% CO2 incubator. .. Transfections SiHa cells were transfected with plasmid vectors, while HeLa cells were transfected with small-interfering RNAs (siRNAs). pCMV6-XL4/5 plasmid vectors containing the TrueClone® human cDNA sequences for human TP53 (NM_000546; cat. no. SC119832), PIK3CA (NM_006218; cat. no. SC116227) or ERBB2 (NM_004448; cat. no. SC128161), and an empty negative control (NC) plasmid vector (cat. no. PCMV6XL5) were obtained from OriGene Technologies, Inc. For plasmid transfections, cells were seeded in 6-well plates (1.5×105 cells/well) and transiently transfected with 1 µg plasmid using Lipofectamine® 3000 transfection reagent (Invitrogen; Thermo Fisher Scientific, Inc.) for 20 min at room temperature and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. siRNAs targeting human ERBB2 (ERBB2-siRNA; cat. no. sc-29405), human PIK3CA (PIK3CA-siRNA; cat. no. sc-39127) and scrambled control (scr-siRNA; cat. no. sc-37007) were obtained from Santa Cruz Biotechnology, Inc. For siRNA transfections, cells were seeded in 6-well plates (2×105 cells/well) and transiently transfected with 80 pmol siRNA using Lipofectamine 3000 transfection reagent for 7 h at 37°C and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. miR-3184-5p (miRBase accession no. MIMAT0015064) mirVana® miRNA mimic (cat. no. 4464066) and mirVana® miRNA inhibitor (cat. no. 4464084), as well as the corresponding controls (cat. nos. .. 4464058 and 4464078, respectively), were obtained from AmbionÒ (Thermo Fisher Scientific, Inc.).

    Incubation:

    Article Title: Erb-B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53-responsive microRNA-3184-5p in cervical cancer cells
    Article Snippet: For in vitro experiments, Mithramycin A dissolved in DMSO at concentrations of 0 (vehicle control), 50 and 100 nM was used to treat cells for 48 h at 37°C in a 5% CO2 incubator. .. Transfections SiHa cells were transfected with plasmid vectors, while HeLa cells were transfected with small-interfering RNAs (siRNAs). pCMV6-XL4/5 plasmid vectors containing the TrueClone® human cDNA sequences for human TP53 (NM_000546; cat. no. SC119832), PIK3CA (NM_006218; cat. no. SC116227) or ERBB2 (NM_004448; cat. no. SC128161), and an empty negative control (NC) plasmid vector (cat. no. PCMV6XL5) were obtained from OriGene Technologies, Inc. For plasmid transfections, cells were seeded in 6-well plates (1.5×105 cells/well) and transiently transfected with 1 µg plasmid using Lipofectamine® 3000 transfection reagent (Invitrogen; Thermo Fisher Scientific, Inc.) for 20 min at room temperature and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. siRNAs targeting human ERBB2 (ERBB2-siRNA; cat. no. sc-29405), human PIK3CA (PIK3CA-siRNA; cat. no. sc-39127) and scrambled control (scr-siRNA; cat. no. sc-37007) were obtained from Santa Cruz Biotechnology, Inc. For siRNA transfections, cells were seeded in 6-well plates (2×105 cells/well) and transiently transfected with 80 pmol siRNA using Lipofectamine 3000 transfection reagent for 7 h at 37°C and then incubated in fresh medium at 37°C for an additional 48 h prior to subsequent experimentation. miR-3184-5p (miRBase accession no. MIMAT0015064) mirVana® miRNA mimic (cat. no. 4464066) and mirVana® miRNA inhibitor (cat. no. 4464084), as well as the corresponding controls (cat. nos. .. 4464058 and 4464078, respectively), were obtained from AmbionÒ (Thermo Fisher Scientific, Inc.).

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  • 80
    OriGene stable cell lines expressing tigar protein
    c-Met inhibitors, AM7 and SU11274, reduce <t>TIGAR</t> expression and cellular NADPH level, leading to apoptosis (A) Apoptosis of NPC cells is associated with p53 and TIGAR downregulation. for antibody sources). Similar results were obtained in 3 independent experiments. (B). AM7 induces dose-dependent reduction of intracellular NADPH in NPC cells. ) and normalized to total protein as μM/min/mg total protein. Percentage reduction of NADPH was calculated with reference to DMSO. Graph show percentage reduction of NADPH level of AM7-treated cells vs DMSO-treated cells (mean ± SEM, n=3). Similar results were obtained in 3 independent experiments. (C) A model c-Met TKI, SU11274 downregulates TIGAR and NADPH levels in NPC cells. HK1-LMP1 and CNE-2 cells were treated with SU11274 or DMSO in complete medium for 48h. Cellular NADPH production was determined as above. The expression levels of TIGAR and p53 were also shown. (D) Overexpression of TIGAR rescues NPC cells from both AM7- and SU11274-mediated growth inhibition. ). Upon confirmation of TIGAR overexpression (by Western blotting for TIGAR; Upper Panel) in these stable cell lines, puromycin selection was removed periodically. <t>Retrovirus-infected</t> stable cell lines from CNE-2 and HONE-1 origin were treated with AM7 (2μM) or SU11274 (5μM) or DMSO in 3% FBS for 72h. Effects of TIGAR overexpression on AM7- or SU11274-induced growth inhibition (as % growth inhibition vs DMSO control) was assayed by MTT assay and presented in the middle and lower panels, respectively. Similar results were obtained in 3 independent experiments.
    Stable Cell Lines Expressing Tigar Protein, supplied by OriGene, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stable cell lines expressing tigar protein/product/OriGene
    Average 80 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    stable cell lines expressing tigar protein - by Bioz Stars, 2021-06
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    93
    OriGene human tp53
    IRF-1 synergistically targets PUMA gene expression with p53. a HCT116TP53 +/+ and HCT116TP53 −/− cells were treated with IFNγ (24 h). Immunofluorescence staining was performed with the indicated antibodies. Representative images are shown, red: IRF1; green: PUMA. b 293 T cells were transfected with pCMV6-xl 5 -hIRF1 (3 μg) or pCMV-xl 5 <t>-TP53</t> (1 μg); and co-transfected with pCMV6-xl 5 -hIRF1 (3 μg) and pCMV-xl 5 -TP53 (1 μg) for 24 h. Total proteins were analyzed by Western blot with the indicated antibodies
    Human Tp53, supplied by OriGene, 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/human tp53/product/OriGene
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human tp53 - by Bioz Stars, 2021-06
    93/100 stars
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    p53  (OriGene)
    93
    OriGene p53
    AXIN1-binding epitopes for CK1ϵ, c-Myc, Pin1, and <t>p53</t> identified by peptide array approach. The microarray slides with AXIN1 peptide library were incubated with the following purified recombinant proteins: CK1ϵ ( A ), c-Myc ( B ), p53 ( C ), and Pin1 ( D ). The charts show normalized signal values from single peptide spots, and the dashed line represents the threshold signal intensity. AXIN1 is schematically depicted above the charts with the numbers and sequences of amino acids defining the particular binding sites. The signals from control glass (antibodies only) were subtracted from the experimental values, and the four strongest signals of at least four consecutive ( i.e. neighboring and overlapping) peptides higher than 10,000 LUs were considered as candidate binding sites; see “Experimental procedures” and main text for more details. For each protein of interest, the average from two to three replicates is shown. hAXIN1 , human AXIN1.
    P53, supplied by OriGene, 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/OriGene
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p53 - by Bioz Stars, 2021-06
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    92
    OriGene p53 shrna
    IFN- γ suppresses Bmf expression to induce autophagy. (A and B) IFN-γ increases protein levels of Beclin-1 and LC3B in AALEB cells (A) and MAECs (B) compared with nontreated (NT) controls as detected by Western blot analysis. (C) AALEB cells treated with IFN-γ for 48 h and infected with 50 MOI of Ad-Bmf CUG or Ad-GFP. Bmf expression inhibits IFN-γ–induced Beclin-1 and LC3B protein levels. (D) Western blot of lung and thymus tissues from bmf +/+ (wild type [WT]) and bmf −/− (knockout [KO]) mice probed for Beclin-1 and LC3B proteins. (E) Western blot analysis of protein extracts from bmf +/+ (wild type) and bmf −/− (knockout) MAECs and MEFs probed for Beclin-1, LC3B, and β-actin. (F) Representative micrographs of bmf +/+ and bmf −/− MAECs and MEFs expressing mCherry-LC3B and cells with punctuate LC3B were quantified from > 50 bmf +/+ and bmf −/− MAECs. (G) Representative electron micrographs of bmf +/+ and bmf −/− MAECs that were cultured in 6-well dishes. Thin sections of cells were analyzed by scanning electron microscopy. The arrowhead denotes an autophagic vesicle, and the arrow denotes a mitochondrion surrounded by a double membrane. Quantification of autophagic vesicles per 100 µm 2 in > 30 each bmf +/+ and bmf −/− MAECs. (H) Quantification of viable bmf +/+ and bmf −/− MEFs maintained in starvation media for 4 or 24 h relative to cell grown in regular media ( n = 3 independent experiments). (I) Quantification of viable bmf +/+ and bmf −/− MEFs 24 h after treatment with the mTOR inhibitor, pp242, at 2.5 µM relative to nontreated control cells ( n = 3 independent experiments). (J) Knockdown of Bmf mRNA using shBmf in <t>p53</t> −/− HCT116 cells reduced Bmf mRNA levels. Western blot analysis of <t>shRNA</t> control (shCtr)– and shBmf-transfected p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. The Western blot is representative of three experiments using three different shBmf constructs. (K) Western blot of IFN-γ–treated p53 +/+ and p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. (L) Immunoprecipitation of protein extracts from IFN-γ–treated and nontreated bmf +/+ and nontreated bmf −/− MEFs using anti–Beclin-1 and Western blot analysis of input and immunoprecipitates (IP) with Bcl-2, Beclin-1, Bmf, and β-actin antibodies. Results are representative of four independent immunoprecipitations. Error bars indicate ±SEM. *, P
    P53 Shrna, supplied by OriGene, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    c-Met inhibitors, AM7 and SU11274, reduce TIGAR expression and cellular NADPH level, leading to apoptosis (A) Apoptosis of NPC cells is associated with p53 and TIGAR downregulation. for antibody sources). Similar results were obtained in 3 independent experiments. (B). AM7 induces dose-dependent reduction of intracellular NADPH in NPC cells. ) and normalized to total protein as μM/min/mg total protein. Percentage reduction of NADPH was calculated with reference to DMSO. Graph show percentage reduction of NADPH level of AM7-treated cells vs DMSO-treated cells (mean ± SEM, n=3). Similar results were obtained in 3 independent experiments. (C) A model c-Met TKI, SU11274 downregulates TIGAR and NADPH levels in NPC cells. HK1-LMP1 and CNE-2 cells were treated with SU11274 or DMSO in complete medium for 48h. Cellular NADPH production was determined as above. The expression levels of TIGAR and p53 were also shown. (D) Overexpression of TIGAR rescues NPC cells from both AM7- and SU11274-mediated growth inhibition. ). Upon confirmation of TIGAR overexpression (by Western blotting for TIGAR; Upper Panel) in these stable cell lines, puromycin selection was removed periodically. Retrovirus-infected stable cell lines from CNE-2 and HONE-1 origin were treated with AM7 (2μM) or SU11274 (5μM) or DMSO in 3% FBS for 72h. Effects of TIGAR overexpression on AM7- or SU11274-induced growth inhibition (as % growth inhibition vs DMSO control) was assayed by MTT assay and presented in the middle and lower panels, respectively. Similar results were obtained in 3 independent experiments.

    Journal: Oncogene

    Article Title: Inhibition of c-Met Downregulates TIGAR Expression and Reduces NADPH Production Leading to Cell Death

    doi: 10.1038/onc.2010.490

    Figure Lengend Snippet: c-Met inhibitors, AM7 and SU11274, reduce TIGAR expression and cellular NADPH level, leading to apoptosis (A) Apoptosis of NPC cells is associated with p53 and TIGAR downregulation. for antibody sources). Similar results were obtained in 3 independent experiments. (B). AM7 induces dose-dependent reduction of intracellular NADPH in NPC cells. ) and normalized to total protein as μM/min/mg total protein. Percentage reduction of NADPH was calculated with reference to DMSO. Graph show percentage reduction of NADPH level of AM7-treated cells vs DMSO-treated cells (mean ± SEM, n=3). Similar results were obtained in 3 independent experiments. (C) A model c-Met TKI, SU11274 downregulates TIGAR and NADPH levels in NPC cells. HK1-LMP1 and CNE-2 cells were treated with SU11274 or DMSO in complete medium for 48h. Cellular NADPH production was determined as above. The expression levels of TIGAR and p53 were also shown. (D) Overexpression of TIGAR rescues NPC cells from both AM7- and SU11274-mediated growth inhibition. ). Upon confirmation of TIGAR overexpression (by Western blotting for TIGAR; Upper Panel) in these stable cell lines, puromycin selection was removed periodically. Retrovirus-infected stable cell lines from CNE-2 and HONE-1 origin were treated with AM7 (2μM) or SU11274 (5μM) or DMSO in 3% FBS for 72h. Effects of TIGAR overexpression on AM7- or SU11274-induced growth inhibition (as % growth inhibition vs DMSO control) was assayed by MTT assay and presented in the middle and lower panels, respectively. Similar results were obtained in 3 independent experiments.

    Article Snippet: Using retrovirus infection, we generated stable cell lines expressing TIGAR protein (human TIGAR gene construct was purchased from Origene, USA) ( ).

    Techniques: Expressing, Over Expression, Inhibition, Western Blot, Stable Transfection, Selection, Infection, MTT Assay

    IRF-1 synergistically targets PUMA gene expression with p53. a HCT116TP53 +/+ and HCT116TP53 −/− cells were treated with IFNγ (24 h). Immunofluorescence staining was performed with the indicated antibodies. Representative images are shown, red: IRF1; green: PUMA. b 293 T cells were transfected with pCMV6-xl 5 -hIRF1 (3 μg) or pCMV-xl 5 -TP53 (1 μg); and co-transfected with pCMV6-xl 5 -hIRF1 (3 μg) and pCMV-xl 5 -TP53 (1 μg) for 24 h. Total proteins were analyzed by Western blot with the indicated antibodies

    Journal: Molecular Medicine

    Article Title: iNOS/NO is required for IRF1 activation in response to liver ischemia-reperfusion in mice

    doi: 10.1186/s10020-020-00182-2

    Figure Lengend Snippet: IRF-1 synergistically targets PUMA gene expression with p53. a HCT116TP53 +/+ and HCT116TP53 −/− cells were treated with IFNγ (24 h). Immunofluorescence staining was performed with the indicated antibodies. Representative images are shown, red: IRF1; green: PUMA. b 293 T cells were transfected with pCMV6-xl 5 -hIRF1 (3 μg) or pCMV-xl 5 -TP53 (1 μg); and co-transfected with pCMV6-xl 5 -hIRF1 (3 μg) and pCMV-xl 5 -TP53 (1 μg) for 24 h. Total proteins were analyzed by Western blot with the indicated antibodies

    Article Snippet: Human TP53 and IRF1 expression plasmids, pCMV6-xl5 -TP53 and pCMV6-xl5-hIRF1 were purchased from Origene, Rockville, MD.

    Techniques: Expressing, Immunofluorescence, Staining, Transfection, Western Blot

    AXIN1-binding epitopes for CK1ϵ, c-Myc, Pin1, and p53 identified by peptide array approach. The microarray slides with AXIN1 peptide library were incubated with the following purified recombinant proteins: CK1ϵ ( A ), c-Myc ( B ), p53 ( C ), and Pin1 ( D ). The charts show normalized signal values from single peptide spots, and the dashed line represents the threshold signal intensity. AXIN1 is schematically depicted above the charts with the numbers and sequences of amino acids defining the particular binding sites. The signals from control glass (antibodies only) were subtracted from the experimental values, and the four strongest signals of at least four consecutive ( i.e. neighboring and overlapping) peptides higher than 10,000 LUs were considered as candidate binding sites; see “Experimental procedures” and main text for more details. For each protein of interest, the average from two to three replicates is shown. hAXIN1 , human AXIN1.

    Journal: The Journal of Biological Chemistry

    Article Title: Analysis of binding interfaces of the human scaffold protein AXIN1 by peptide microarrays

    doi: 10.1074/jbc.RA118.005127

    Figure Lengend Snippet: AXIN1-binding epitopes for CK1ϵ, c-Myc, Pin1, and p53 identified by peptide array approach. The microarray slides with AXIN1 peptide library were incubated with the following purified recombinant proteins: CK1ϵ ( A ), c-Myc ( B ), p53 ( C ), and Pin1 ( D ). The charts show normalized signal values from single peptide spots, and the dashed line represents the threshold signal intensity. AXIN1 is schematically depicted above the charts with the numbers and sequences of amino acids defining the particular binding sites. The signals from control glass (antibodies only) were subtracted from the experimental values, and the four strongest signals of at least four consecutive ( i.e. neighboring and overlapping) peptides higher than 10,000 LUs were considered as candidate binding sites; see “Experimental procedures” and main text for more details. For each protein of interest, the average from two to three replicates is shown. hAXIN1 , human AXIN1.

    Article Snippet: Then the experimental slide was incubated overnight with 10 μg/ml recombinant protein, CK1ϵ (OriGene Technologies, TP302436), p53 (OriGene Technologies, TP300003) Pin1 (OriGene Technologies, TP302543), or c-Myc (Abnova, H00004609-P01), in SmartBlock solution (final volume, 300 μl) at 4 °C.

    Techniques: Binding Assay, Peptide Microarray, Microarray, Incubation, Purification, Recombinant

    IFN- γ suppresses Bmf expression to induce autophagy. (A and B) IFN-γ increases protein levels of Beclin-1 and LC3B in AALEB cells (A) and MAECs (B) compared with nontreated (NT) controls as detected by Western blot analysis. (C) AALEB cells treated with IFN-γ for 48 h and infected with 50 MOI of Ad-Bmf CUG or Ad-GFP. Bmf expression inhibits IFN-γ–induced Beclin-1 and LC3B protein levels. (D) Western blot of lung and thymus tissues from bmf +/+ (wild type [WT]) and bmf −/− (knockout [KO]) mice probed for Beclin-1 and LC3B proteins. (E) Western blot analysis of protein extracts from bmf +/+ (wild type) and bmf −/− (knockout) MAECs and MEFs probed for Beclin-1, LC3B, and β-actin. (F) Representative micrographs of bmf +/+ and bmf −/− MAECs and MEFs expressing mCherry-LC3B and cells with punctuate LC3B were quantified from > 50 bmf +/+ and bmf −/− MAECs. (G) Representative electron micrographs of bmf +/+ and bmf −/− MAECs that were cultured in 6-well dishes. Thin sections of cells were analyzed by scanning electron microscopy. The arrowhead denotes an autophagic vesicle, and the arrow denotes a mitochondrion surrounded by a double membrane. Quantification of autophagic vesicles per 100 µm 2 in > 30 each bmf +/+ and bmf −/− MAECs. (H) Quantification of viable bmf +/+ and bmf −/− MEFs maintained in starvation media for 4 or 24 h relative to cell grown in regular media ( n = 3 independent experiments). (I) Quantification of viable bmf +/+ and bmf −/− MEFs 24 h after treatment with the mTOR inhibitor, pp242, at 2.5 µM relative to nontreated control cells ( n = 3 independent experiments). (J) Knockdown of Bmf mRNA using shBmf in p53 −/− HCT116 cells reduced Bmf mRNA levels. Western blot analysis of shRNA control (shCtr)– and shBmf-transfected p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. The Western blot is representative of three experiments using three different shBmf constructs. (K) Western blot of IFN-γ–treated p53 +/+ and p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. (L) Immunoprecipitation of protein extracts from IFN-γ–treated and nontreated bmf +/+ and nontreated bmf −/− MEFs using anti–Beclin-1 and Western blot analysis of input and immunoprecipitates (IP) with Bcl-2, Beclin-1, Bmf, and β-actin antibodies. Results are representative of four independent immunoprecipitations. Error bars indicate ±SEM. *, P

    Journal: The Journal of Cell Biology

    Article Title: Deacetylation of p53 induces autophagy by suppressing Bmf expression

    doi: 10.1083/jcb.201205064

    Figure Lengend Snippet: IFN- γ suppresses Bmf expression to induce autophagy. (A and B) IFN-γ increases protein levels of Beclin-1 and LC3B in AALEB cells (A) and MAECs (B) compared with nontreated (NT) controls as detected by Western blot analysis. (C) AALEB cells treated with IFN-γ for 48 h and infected with 50 MOI of Ad-Bmf CUG or Ad-GFP. Bmf expression inhibits IFN-γ–induced Beclin-1 and LC3B protein levels. (D) Western blot of lung and thymus tissues from bmf +/+ (wild type [WT]) and bmf −/− (knockout [KO]) mice probed for Beclin-1 and LC3B proteins. (E) Western blot analysis of protein extracts from bmf +/+ (wild type) and bmf −/− (knockout) MAECs and MEFs probed for Beclin-1, LC3B, and β-actin. (F) Representative micrographs of bmf +/+ and bmf −/− MAECs and MEFs expressing mCherry-LC3B and cells with punctuate LC3B were quantified from > 50 bmf +/+ and bmf −/− MAECs. (G) Representative electron micrographs of bmf +/+ and bmf −/− MAECs that were cultured in 6-well dishes. Thin sections of cells were analyzed by scanning electron microscopy. The arrowhead denotes an autophagic vesicle, and the arrow denotes a mitochondrion surrounded by a double membrane. Quantification of autophagic vesicles per 100 µm 2 in > 30 each bmf +/+ and bmf −/− MAECs. (H) Quantification of viable bmf +/+ and bmf −/− MEFs maintained in starvation media for 4 or 24 h relative to cell grown in regular media ( n = 3 independent experiments). (I) Quantification of viable bmf +/+ and bmf −/− MEFs 24 h after treatment with the mTOR inhibitor, pp242, at 2.5 µM relative to nontreated control cells ( n = 3 independent experiments). (J) Knockdown of Bmf mRNA using shBmf in p53 −/− HCT116 cells reduced Bmf mRNA levels. Western blot analysis of shRNA control (shCtr)– and shBmf-transfected p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. The Western blot is representative of three experiments using three different shBmf constructs. (K) Western blot of IFN-γ–treated p53 +/+ and p53 −/− HCT116 cells probed with Beclin-1, LC3B, and β-actin antibodies. (L) Immunoprecipitation of protein extracts from IFN-γ–treated and nontreated bmf +/+ and nontreated bmf −/− MEFs using anti–Beclin-1 and Western blot analysis of input and immunoprecipitates (IP) with Bcl-2, Beclin-1, Bmf, and β-actin antibodies. Results are representative of four independent immunoprecipitations. Error bars indicate ±SEM. *, P

    Article Snippet: The retroviral silencing vector encoding for p53 shRNA and the control vector were purchased from OriGene.

    Techniques: Expressing, Western Blot, Infection, Knock-Out, Mouse Assay, Cell Culture, Electron Microscopy, shRNA, Transfection, Construct, Immunoprecipitation