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p73 antibody img 259a (Novus Biologicals)

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Novus Biologicals p73 antibody img 259a

( A ) Quantification: Proteins were extracted from C2C12 myoblasts treated with compounds: FCCP, Tunicamycin (Tun), Etoposide (Eto), menadione (Men). Western blot analysis revealed TAp63 expression. Bars correspond to means with SD (n = 3). *p<0.01. ( B ) C2C12 myoblasts were transfected with expression vectors encoding transcription factors involved in the ER or mitochondrial stress pathway (CHOP, ATF6, ATF4, XBP1s). RNA levels for TA isoforms of Trp63 , TA isoforms of <t>P73</t> and P53 were followed by RT-qPCR. Bars represent means (relative induction versus Ct) with standard deviation (n = 3).*p<0.01. DOI: http://dx.doi.org/10.7554/eLife.10528.016

P73 Antibody Img 259a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p73 antibody img 259a - by Bioz Stars, 2026-03

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1) Product Images from "Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63"

Article Title: Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63

Journal: eLife

doi: 10.7554/eLife.10528

Figure Legend Snippet: ( A ) Quantification: Proteins were extracted from C2C12 myoblasts treated with compounds: FCCP, Tunicamycin (Tun), Etoposide (Eto), menadione (Men). Western blot analysis revealed TAp63 expression. Bars correspond to means with SD (n = 3). *p<0.01. ( B ) C2C12 myoblasts were transfected with expression vectors encoding transcription factors involved in the ER or mitochondrial stress pathway (CHOP, ATF6, ATF4, XBP1s). RNA levels for TA isoforms of Trp63 , TA isoforms of P73 and P53 were followed by RT-qPCR. Bars represent means (relative induction versus Ct) with standard deviation (n = 3).*p<0.01. DOI: http://dx.doi.org/10.7554/eLife.10528.016

Techniques Used: Western Blot, Expressing, Transfection, Quantitative RT-PCR, Standard Deviation

( A ) mRNA levels of Trim63 in C2C12 cells following transfection with siRNA control and siRNA directed against p73, p53 and a mix of siRNA against P53, and the TA isoforms of Trp63 and P73 (siMIX). Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( B ) mRNA level for TA isoforms of Trp63 , TA isoforms of P73 and P53 in C2C12 cells following transfection with siRNA control and siRNA directed against p63, p73, and p53. Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( C, D ) Chromatin immunoprecipitation (ChIP) assay was performed on the Trim63 promoter using RT-qPCR on RE1/2 and RE4. p53 immunoprecipitation (C) was performed using p53 antibody IC12 (Cell Signalling), p73 immunoprecipitation was performed using p73 antibody IMG-259a (Imgenex). Bars correspond to means with SD (n = 3). *p<0.01 as calculated by a one-way ANOVA test followed by a Tukey post-test. DOI: http://dx.doi.org/10.7554/eLife.10528.019

Figure Legend Snippet: ( A ) mRNA levels of Trim63 in C2C12 cells following transfection with siRNA control and siRNA directed against p73, p53 and a mix of siRNA against P53, and the TA isoforms of Trp63 and P73 (siMIX). Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( B ) mRNA level for TA isoforms of Trp63 , TA isoforms of P73 and P53 in C2C12 cells following transfection with siRNA control and siRNA directed against p63, p73, and p53. Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( C, D ) Chromatin immunoprecipitation (ChIP) assay was performed on the Trim63 promoter using RT-qPCR on RE1/2 and RE4. p53 immunoprecipitation (C) was performed using p53 antibody IC12 (Cell Signalling), p73 immunoprecipitation was performed using p73 antibody IMG-259a (Imgenex). Bars correspond to means with SD (n = 3). *p<0.01 as calculated by a one-way ANOVA test followed by a Tukey post-test. DOI: http://dx.doi.org/10.7554/eLife.10528.019

Techniques Used: Transfection, Control, Standard Deviation, Chromatin Immunoprecipitation, Quantitative RT-PCR, Immunoprecipitation

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Journal: eLife

Article Title: Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63

doi: 10.7554/eLife.10528

Figure Lengend Snippet: ( A ) Quantification: Proteins were extracted from C2C12 myoblasts treated with compounds: FCCP, Tunicamycin (Tun), Etoposide (Eto), menadione (Men). Western blot analysis revealed TAp63 expression. Bars correspond to means with SD (n = 3). *p<0.01. ( B ) C2C12 myoblasts were transfected with expression vectors encoding transcription factors involved in the ER or mitochondrial stress pathway (CHOP, ATF6, ATF4, XBP1s). RNA levels for TA isoforms of Trp63 , TA isoforms of P73 and P53 were followed by RT-qPCR. Bars represent means (relative induction versus Ct) with standard deviation (n = 3).*p<0.01. DOI: http://dx.doi.org/10.7554/eLife.10528.016

Article Snippet: *p<0.01. ( C, D ) Chromatin immunoprecipitation (ChIP) assay was performed on the Trim63 promoter using RT-qPCR on RE1/2 and RE4. p53 immunoprecipitation (C) was performed using p53 antibody IC12 (Cell Signalling), p73 immunoprecipitation was performed using p73 antibody IMG-259a (Imgenex).

Techniques: Western Blot, Expressing, Transfection, Quantitative RT-PCR, Standard Deviation

Journal: eLife

Article Title: Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63

doi: 10.7554/eLife.10528

Figure Lengend Snippet: ( A ) mRNA levels of Trim63 in C2C12 cells following transfection with siRNA control and siRNA directed against p73, p53 and a mix of siRNA against P53, and the TA isoforms of Trp63 and P73 (siMIX). Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( B ) mRNA level for TA isoforms of Trp63 , TA isoforms of P73 and P53 in C2C12 cells following transfection with siRNA control and siRNA directed against p63, p73, and p53. Bars represent means (relative induction versus Ct) with standard deviation (n = 3). *p<0.01. ( C, D ) Chromatin immunoprecipitation (ChIP) assay was performed on the Trim63 promoter using RT-qPCR on RE1/2 and RE4. p53 immunoprecipitation (C) was performed using p53 antibody IC12 (Cell Signalling), p73 immunoprecipitation was performed using p73 antibody IMG-259a (Imgenex). Bars correspond to means with SD (n = 3). *p<0.01 as calculated by a one-way ANOVA test followed by a Tukey post-test. DOI: http://dx.doi.org/10.7554/eLife.10528.019

Techniques: Transfection, Control, Standard Deviation, Chromatin Immunoprecipitation, Quantitative RT-PCR, Immunoprecipitation

control = empty vector. b) Induction of p21-luc by TAp73α and its inhibition by co-expression of increasing amounts of ΔNp73. c) Induction of PAI-1-luc by TAp73α and its enhancement by co-expression of increasing amounts of ΔNp73. d) Activation of the PAI-1-luc promoter with a mutated p53 Binding Element: induction of promoter activity by p53 and TAp73 depends on an intact p53 binding element in the promoter, whilst ΔNp73 shows activity even if the p53 binding element is lacking. Transfected cells were cultured in the presence of 1 ng/ml TGF-β1 for 24 hours where indicated (right). e) Induction of Smad Binding Elements by p53 or p73 variants and/or TGF-β. Only ΔNp73 shows activity. Transfected cells were cultured in the presence of 1 ng/ml TGF-β1 for 24 hours. control = empty vector. TAp73γ and δ forms are shown only in and were omitted in the rest of the figures for simplicity; they always showed similar results as TAp73.

Journal: PLoS ONE

Article Title: ΔNp73 Enhances Promoter Activity of TGF-β Induced Genes

doi: 10.1371/journal.pone.0050815

Figure Lengend Snippet: control = empty vector. b) Induction of p21-luc by TAp73α and its inhibition by co-expression of increasing amounts of ΔNp73. c) Induction of PAI-1-luc by TAp73α and its enhancement by co-expression of increasing amounts of ΔNp73. d) Activation of the PAI-1-luc promoter with a mutated p53 Binding Element: induction of promoter activity by p53 and TAp73 depends on an intact p53 binding element in the promoter, whilst ΔNp73 shows activity even if the p53 binding element is lacking. Transfected cells were cultured in the presence of 1 ng/ml TGF-β1 for 24 hours where indicated (right). e) Induction of Smad Binding Elements by p53 or p73 variants and/or TGF-β. Only ΔNp73 shows activity. Transfected cells were cultured in the presence of 1 ng/ml TGF-β1 for 24 hours. control = empty vector. TAp73γ and δ forms are shown only in and were omitted in the rest of the figures for simplicity; they always showed similar results as TAp73.

Article Snippet: Membranes were reacted with the following primary antibodies: α-V5 (Invitrogen) for V5-tagged Smad3, α-HA (Covance) for HA-tagged p73, PAN-p73 IMG-259A (Imgenex), α-GFP (Santa Cruz) for tagged Smad4, and α-Smad3 clone 2C12 (Sigma-Aldrich) for endogenous Smad3, followed by the appropriate HRP-conjugated secondary antibody and ECL detection.

Techniques: Control, Plasmid Preparation, Inhibition, Expressing, Activation Assay, Binding Assay, Activity Assay, Transfection, Cell Culture

a) Luciferase assays comparing the effect of ΔNp73 on Hep3B cells versus Hek293 cells using SBE-luc as reporter, cotransfected with either empty vector or 10 ng/well ΔNp73, and/or treated with 1 ng/ml TGF-β1. b) Luciferase assay of MDA-MB-468 cells (deficient for Smad4) transfected with 400 ng/well PAI1-luc, 100 ng/well empty vector (to compensate for Smad4 plasmid in ) and either 10 ng/well empty vector (control), TAp73 or ΔNp73. Cells were grown with or without TGF-β1. c) Luciferase assay of MDA-MB-468 cells (deficient for Smad4) transfected with 400 ng/well SBE-luc, 100 ng/well Smad4 and 10 ng/well of either empty vector (control) or ΔNp73. Cells were grown in the presence of TGF-β1 where indicated. ** p<0.05 and *p<0.10 in a two-tailed T-test. d) Immunoblot analysis using a PAN-p73 specific antibody using lysates of Hek293 cells transfected with either empty pSuper vector as control (C1 or C2) or pSuper vectors expressing shRNA directed to the ΔN specific part of ΔNp73, a lysate of Hek293 cells transfected with a plasmid expressing HA-tagged ΔNp73α was used to serve as marker for the height of ΔNp73α. The bands corresponding to this height are shown additionally with a light balance appropriate for this band. Two ΔN p73 targeting sequences were used: ΔN1 and ΔN2. The PAN-p73 antibody detected multiple bands including the ΔNp73α variant. However, only a few specific bands, including a band with the height of ΔNp73α, were reduced whereas other bands were not affected, indicating that ΔNp73 variants were specifically downregulated. e) Luciferase assays of Hek293 cells transfected with SBE-luc and either pSuper empty vector control or pSuper ΔN1 and ΔN2 (combination), showing that (partial) ΔNp73 specific downregulation significantly decreases TGF-β signaling. ** p<0.05 in a two-tailed T-test. f) QPCR analysis of PAI-1 mRNA in tetracycline regulated ΔNp73 expressing cells, left untreated or after induction of ΔNp73. g) QPCR analysis of Col1a1 mRNA in tetracycline regulated ΔNp73 expressing cells left untreated or after induction of ΔNp73. ** p<0.05 in a two-tailed T-test.

Journal: PLoS ONE

Article Title: ΔNp73 Enhances Promoter Activity of TGF-β Induced Genes

doi: 10.1371/journal.pone.0050815

Figure Lengend Snippet: a) Luciferase assays comparing the effect of ΔNp73 on Hep3B cells versus Hek293 cells using SBE-luc as reporter, cotransfected with either empty vector or 10 ng/well ΔNp73, and/or treated with 1 ng/ml TGF-β1. b) Luciferase assay of MDA-MB-468 cells (deficient for Smad4) transfected with 400 ng/well PAI1-luc, 100 ng/well empty vector (to compensate for Smad4 plasmid in ) and either 10 ng/well empty vector (control), TAp73 or ΔNp73. Cells were grown with or without TGF-β1. c) Luciferase assay of MDA-MB-468 cells (deficient for Smad4) transfected with 400 ng/well SBE-luc, 100 ng/well Smad4 and 10 ng/well of either empty vector (control) or ΔNp73. Cells were grown in the presence of TGF-β1 where indicated. ** p<0.05 and *p<0.10 in a two-tailed T-test. d) Immunoblot analysis using a PAN-p73 specific antibody using lysates of Hek293 cells transfected with either empty pSuper vector as control (C1 or C2) or pSuper vectors expressing shRNA directed to the ΔN specific part of ΔNp73, a lysate of Hek293 cells transfected with a plasmid expressing HA-tagged ΔNp73α was used to serve as marker for the height of ΔNp73α. The bands corresponding to this height are shown additionally with a light balance appropriate for this band. Two ΔN p73 targeting sequences were used: ΔN1 and ΔN2. The PAN-p73 antibody detected multiple bands including the ΔNp73α variant. However, only a few specific bands, including a band with the height of ΔNp73α, were reduced whereas other bands were not affected, indicating that ΔNp73 variants were specifically downregulated. e) Luciferase assays of Hek293 cells transfected with SBE-luc and either pSuper empty vector control or pSuper ΔN1 and ΔN2 (combination), showing that (partial) ΔNp73 specific downregulation significantly decreases TGF-β signaling. ** p<0.05 in a two-tailed T-test. f) QPCR analysis of PAI-1 mRNA in tetracycline regulated ΔNp73 expressing cells, left untreated or after induction of ΔNp73. g) QPCR analysis of Col1a1 mRNA in tetracycline regulated ΔNp73 expressing cells left untreated or after induction of ΔNp73. ** p<0.05 in a two-tailed T-test.

Techniques: Luciferase, Plasmid Preparation, Transfection, Control, Two Tailed Test, Western Blot, Expressing, shRNA, Marker, Variant Assay

Eighty-six genes (brown) were down regulated in the absence of all three p53 family members. A number of genes were down regulated in the absence of each p53 family member individually; 109 in p53 deficient cells (red), 148 in p63 deficient cells (yellow), and 131 in p73 deficient cells (blue). Several genes were down regulated in the absence of two family members; 47 in the absence of p53 and p63 (orange), 58 in the absence of p63 and p73 (green), and 41 in the absence of p53 and p73 (purple).

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: Eighty-six genes (brown) were down regulated in the absence of all three p53 family members. A number of genes were down regulated in the absence of each p53 family member individually; 109 in p53 deficient cells (red), 148 in p63 deficient cells (yellow), and 131 in p73 deficient cells (blue). Several genes were down regulated in the absence of two family members; 47 in the absence of p53 and p63 (orange), 58 in the absence of p63 and p73 (green), and 41 in the absence of p53 and p73 (purple).

Article Snippet: Slides were incubated with primary antibodies for p63 (4A4, Santa Cruz), p73 (IMG-259A, Imgenex), Rad51 (clone 51RAD01, Neomarkers), or BRCA2 (clone H-300), Santa Cruz). at a dilution of 1∶100 for 18 hours at 4 deg C. Detection was performed using the Vectastain kit (Vector Labs) followed by the VIP kit or DAB kit (Vector Labs) and counterstained with methyl green (Vector Labs).

Techniques:

Each row represents the specified gene. Each column represents the expression level of a specified knock out MEF line relative to the expression level of wild-type MEFs after DNA damage. The red color indicates upregulation, the green color indicates down regulation, while black indicates no significant change of the indicated gene expression. Clustering based on Euclidean distance indicates that p63- and p73- deficient E1A MEFs are more similar to each other than to p53−/− E1A MEFs. Genes of interest are listed in boxes and are associated with their corresponding location on the heatmap.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: Each row represents the specified gene. Each column represents the expression level of a specified knock out MEF line relative to the expression level of wild-type MEFs after DNA damage. The red color indicates upregulation, the green color indicates down regulation, while black indicates no significant change of the indicated gene expression. Clustering based on Euclidean distance indicates that p63- and p73- deficient E1A MEFs are more similar to each other than to p53−/− E1A MEFs. Genes of interest are listed in boxes and are associated with their corresponding location on the heatmap.

Techniques: Expressing, Knock-Out

p53 family response elements assayed by ChIP.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: p53 family response elements assayed by ChIP.

Techniques:

Real time PCR analysis of E1A MEFs of the following genotypes (wild-type, p53−/− , p63−/−, p73−/− and p63−/−;p73−/− ) after treatment with (A) doxorubicin (0.34 µM) for 12 hours or (B) γ radiation (12 hours). The Y-axis shows the fold induction. Bars represent 3 MEF lines for each genotype, each performed in triplicate. Data represent the mean ± SEM. The asterisk denotes statistical significance compared to wild-type, p<0.001.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: Real time PCR analysis of E1A MEFs of the following genotypes (wild-type, p53−/− , p63−/−, p73−/− and p63−/−;p73−/− ) after treatment with (A) doxorubicin (0.34 µM) for 12 hours or (B) γ radiation (12 hours). The Y-axis shows the fold induction. Bars represent 3 MEF lines for each genotype, each performed in triplicate. Data represent the mean ± SEM. The asterisk denotes statistical significance compared to wild-type, p<0.001.

Techniques: Real-time Polymerase Chain Reaction

(A) Western blot analysis for Rad51 using whole cell lysates from wild-type and p63−/−;p73−/− MEFs treated with 0 Gy or 10 min (m), 30 m, 1 hour (h), 2 h and 4 h after 5 Gy of gamma irradiation. Actin was used as a control for equal loading. (B–I) Immunohistochemistry (IHC) of normal mammary tissue or mammary adenocarcinomas from p63+/−;p73+/− mice using antibodies as follows: (B) normal mammary tissue from p63+/−;p73+/− mouse using Rad51 antibody, (C) mammary adenocarcinoma from p63+/−;p73+/− mouse using Rad51 antibody, (D) normal mammary tissue from p63+/−;p73+/− mouse using BRCA2 antibody, (E) mammary adenocarcinoma from p63+/−;p73+/− mouse using BRCA2 antibody, (F) normal mammary tissue from p63+/−;p73+/− mouse using p63 antibody, (G) mammary adenocarcinoma from p63+/−;p73+/− mouse using p63 antibody, (H) normal mammary tissue from p63+/−;p73+/− mouse using p73 antibody, (I) mammary adenocarcinoma from p63+/−;p73+/− mouse using p73 antibody.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: (A) Western blot analysis for Rad51 using whole cell lysates from wild-type and p63−/−;p73−/− MEFs treated with 0 Gy or 10 min (m), 30 m, 1 hour (h), 2 h and 4 h after 5 Gy of gamma irradiation. Actin was used as a control for equal loading. (B–I) Immunohistochemistry (IHC) of normal mammary tissue or mammary adenocarcinomas from p63+/−;p73+/− mice using antibodies as follows: (B) normal mammary tissue from p63+/−;p73+/− mouse using Rad51 antibody, (C) mammary adenocarcinoma from p63+/−;p73+/− mouse using Rad51 antibody, (D) normal mammary tissue from p63+/−;p73+/− mouse using BRCA2 antibody, (E) mammary adenocarcinoma from p63+/−;p73+/− mouse using BRCA2 antibody, (F) normal mammary tissue from p63+/−;p73+/− mouse using p63 antibody, (G) mammary adenocarcinoma from p63+/−;p73+/− mouse using p63 antibody, (H) normal mammary tissue from p63+/−;p73+/− mouse using p73 antibody, (I) mammary adenocarcinoma from p63+/−;p73+/− mouse using p73 antibody.

Techniques: Western Blot, Irradiation, Control, Immunohistochemistry

Chromatin immunoprecipitation (ChIP) analysis using wild-type E1A MEFs (WT) and E1A MEFs deficient for the p53 family members ( p53−/− , p63−/− and p73−/− ) before (U) and after treatment with doxorubicin (D) for 12 hours. Antibodies used to immunoprecipitate protein-DNA complexes in each cell line are shown in various colors: p53 (red), p63 (blue), and p73 (green). Total input chromatin is shown for each sample (input). Each ChIP was performed using 3 independent MEF lines in triplicate.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: Chromatin immunoprecipitation (ChIP) analysis using wild-type E1A MEFs (WT) and E1A MEFs deficient for the p53 family members ( p53−/− , p63−/− and p73−/− ) before (U) and after treatment with doxorubicin (D) for 12 hours. Antibodies used to immunoprecipitate protein-DNA complexes in each cell line are shown in various colors: p53 (red), p63 (blue), and p73 (green). Total input chromatin is shown for each sample (input). Each ChIP was performed using 3 independent MEF lines in triplicate.

Techniques: Chromatin Immunoprecipitation

Bar graphs showing fold induction for each luciferase reporter gene in (A–D) p63−/−; p73−/− or (E,F) p53−/−;p73−/− primary MEFs. Reporter genes used are as follows: (A,E) pGL3-Rad51-1 containing the binding elements in intron 1, (B) pGL3-Rad51-2 containing the binding elements in intron 2, (C,F) pGL3-BRCA2 containing the binding element in intron 2, and (D) pGL3-mre-11 containing the binding element in intron 1. Pluses above each bar graph indicate which isoforms of p63 or p73 were transfected in cells with the firefly-luciferase reporter genes. Renilla-luciferase was used as a control for transfection efficiency, and pPERP-luc was used as a positive control. Each experiment was performed 6 times using 3 independent MEF lines. Data are represented as the mean ± SEM.

Journal: PLoS Genetics

Article Title: p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair

doi: 10.1371/journal.pgen.1000680

Figure Lengend Snippet: Bar graphs showing fold induction for each luciferase reporter gene in (A–D) p63−/−; p73−/− or (E,F) p53−/−;p73−/− primary MEFs. Reporter genes used are as follows: (A,E) pGL3-Rad51-1 containing the binding elements in intron 1, (B) pGL3-Rad51-2 containing the binding elements in intron 2, (C,F) pGL3-BRCA2 containing the binding element in intron 2, and (D) pGL3-mre-11 containing the binding element in intron 1. Pluses above each bar graph indicate which isoforms of p63 or p73 were transfected in cells with the firefly-luciferase reporter genes. Renilla-luciferase was used as a control for transfection efficiency, and pPERP-luc was used as a positive control. Each experiment was performed 6 times using 3 independent MEF lines. Data are represented as the mean ± SEM.

Techniques: Luciferase, Binding Assay, Transfection, Control, Positive Control

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1) Product Images from "Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63"

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