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93
Cusabio anti p53 antibody p53
WSB2 promotes the proliferation and migration of breast cancer cells. (A) Reverse transcription-quantitative PCR and (B) western blotting were used to detect the effect of WSB2 overexpression in MDA-MB-231 and MCF-7 cells. (C) Viability of MDA-MB-231 and MCF-7 cells was evaluated using a CCK-8 assay. (D) Representative images and (E) the quantification of the number of MDA-MB-231 and MCF-7 cells in the S phase evaluated using an 5 ethynyl-2′-deoxyuridine assay. (F) Representative images of colony formation ability of MDA-MB-231 and MCF-7cells. (G) Representative images and (H) quantification of wound healing and (I) colony formation ability of MDA-MB-231 and MCF-7cells. (J) Transwell assays to determine the migration ability of MDA-MB-231and MCF-7cells. (K) ERK1/2, <t>p53</t> and PCNA and (L) Snail, E-cadherin and Vimentin protein levels in MDA-MB-231 and MCF-7 cells were detected using western blotting. *P<0.05, **P<0.01, ***P<0.001. WSB2, WD repeat and SOCS box containing 2.
Anti P53 Antibody P53, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
anti p53 antibody p53 - by Bioz Stars, 2026-03
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96
Proteintech rabbit anti human p53
JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and <t>p53-related</t> apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC
Rabbit Anti Human P53, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1 article reviews
rabbit anti human p53 - by Bioz Stars, 2026-03
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97
Cell Signaling Technology Inc anti human p53 antibody
JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and <t>p53-related</t> apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC
Anti Human P53 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti human p53 antibody/product/Cell Signaling Technology Inc
Average 97 stars, based on 1 article reviews
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Cell Signaling Technology Inc anti human p53 rabbit polyclonal antibody
JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and <t>p53-related</t> apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC
Anti Human P53 Rabbit Polyclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti human p53 rabbit polyclonal antibody/product/Cell Signaling Technology Inc
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Cell Signaling Technology Inc human p53
JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and <t>p53-related</t> apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC
Human P53, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human p53/product/Cell Signaling Technology Inc
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Cell Signaling Technology Inc rabbit anti human p53

Rabbit Anti Human P53, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc rabbit anti human p53 cell signaling

Rabbit Anti Human P53 Cell Signaling, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


WSB2 promotes the proliferation and migration of breast cancer cells. (A) Reverse transcription-quantitative PCR and (B) western blotting were used to detect the effect of WSB2 overexpression in MDA-MB-231 and MCF-7 cells. (C) Viability of MDA-MB-231 and MCF-7 cells was evaluated using a CCK-8 assay. (D) Representative images and (E) the quantification of the number of MDA-MB-231 and MCF-7 cells in the S phase evaluated using an 5 ethynyl-2′-deoxyuridine assay. (F) Representative images of colony formation ability of MDA-MB-231 and MCF-7cells. (G) Representative images and (H) quantification of wound healing and (I) colony formation ability of MDA-MB-231 and MCF-7cells. (J) Transwell assays to determine the migration ability of MDA-MB-231and MCF-7cells. (K) ERK1/2, p53 and PCNA and (L) Snail, E-cadherin and Vimentin protein levels in MDA-MB-231 and MCF-7 cells were detected using western blotting. *P<0.05, **P<0.01, ***P<0.001. WSB2, WD repeat and SOCS box containing 2.

Journal: Molecular Medicine Reports

Article Title: Pan-cancer analysis of the carcinogenic role of WSB2 in human tumors

doi: 10.3892/mmr.2025.13625

Figure Lengend Snippet: WSB2 promotes the proliferation and migration of breast cancer cells. (A) Reverse transcription-quantitative PCR and (B) western blotting were used to detect the effect of WSB2 overexpression in MDA-MB-231 and MCF-7 cells. (C) Viability of MDA-MB-231 and MCF-7 cells was evaluated using a CCK-8 assay. (D) Representative images and (E) the quantification of the number of MDA-MB-231 and MCF-7 cells in the S phase evaluated using an 5 ethynyl-2′-deoxyuridine assay. (F) Representative images of colony formation ability of MDA-MB-231 and MCF-7cells. (G) Representative images and (H) quantification of wound healing and (I) colony formation ability of MDA-MB-231 and MCF-7cells. (J) Transwell assays to determine the migration ability of MDA-MB-231and MCF-7cells. (K) ERK1/2, p53 and PCNA and (L) Snail, E-cadherin and Vimentin protein levels in MDA-MB-231 and MCF-7 cells were detected using western blotting. *P<0.05, **P<0.01, ***P<0.001. WSB2, WD repeat and SOCS box containing 2.

Article Snippet: Standard technique was used to carry out western blotting ( ) and the following specific primary antibodies were used: Anti-WSB2 (cat. no. ab127176; Abcam, 1:2,000), anti-GADPH (cat. no. CSB-MA000071Mom; Cusabio Technology, LLC, 1:10,000), anti-β-Actin (cat. no. AC026; ABclonal Biotech Co., Ltd. 1:10,000 dilution), anti-HA-tag (cat. no. B1021; Suzhou Botelon Immunotechnology Co., Ltd. 1:5,000), anti-E-cadherin (cat. no. BD-PT1454; Suzhou Botelon Immunotechnology Co., Ltd.; 1:500 dilution), anti-proliferating cell nuclear antigen (PCNA; cat. no. D220014-0025; Sangon Biotech Co., Ltd. 1:1,000 dilution), anti-Vimentin (cat. no. BD-PB4686; Suzhou Botelon Immunotechnology Co., Ltd. 1:500), anti-p53 antibody (p53) (cat. no. CSB-PA07889A0Rb; Cusabio Technology, LLC.

Techniques: Migration, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, CCK-8 Assay

JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and p53-related apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC

Journal: BMC Biology

Article Title: m6A-modified circZNF548 regulates exosomal miR-7108-3p to activate CD3 + CD8 + T cells and suppress NSCLC growth by JMY

doi: 10.1186/s12915-025-02355-z

Figure Lengend Snippet: JMY is a target of miR-7108-3p. A The binding sites of JMY-3’-UTR (Mu-JMY with mutant site) and miR-7108-3p. B miR-7108-3p regulated luciferase expression in the luci-JMY-3’-UTR- or luci-Mu-JMY-3’-UTR-treated A549 or H1975 cells. Data are presented as the mean ± SD. **p < 0.01; Student’s t-test. ns, no significance. C Immunoblotting analyzing the expression of JMY and p53-related apoptotic genes in A549 cells. D - F JMY levels in miR-7108-3p-treated and circZNF548-treated cells was detected by immunofluorescence. Bar = 125 μm. G JMY-3’-UTR recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell growth. Data are presented as the mean ± SD. **p < 0.01; ANOVA. H , I JMY recovery affected the role of miR-7108-3p and inhibitor miR-7108-3p in cell migration, respectively. bar = 100 μm. Data are presented as the mean ± SD. **p < 0.01; ANOVA. J Immunohistochemical staining showed JMY levels increased in adjacent tissues. The score of staining was shown below the figure. bar = 125 μm. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. K qRT-PCR analysis showed that JMY expression was low in NSCLC tissues. Data were present as median (interquartile range), **p < 0.01; Mann–Whitney U test. L The relationship between JMY expression and miR-7108-3p levels. M The relationship between JMY and circZNF548 levels. N Overall survival analysis of JMY expression in patients with NSCLC

Article Snippet: Membranes were incubated overnight at 4 °C with the following primary antibodies: rabbit anti-human GAPDH (1:3000, BS65656, Bioworld, MN, USA), rabbit anti-human P53 (1:1000, 60,283–2-lg, Proteintech, PA, USA), rabbit anti-human JMY (1:500, 25,098–1-AP, Proteintech), rabbit anti-human Bax (1:500, BS79706, Bioworld), rabbit anti-human Bcl2 (1:500, BZ16777, Bioworld), rabbit anti-human CD8a (1:500, 48,750–1, Signalway Antibody, MD, USA).

Techniques: Binding Assay, Mutagenesis, Luciferase, Expressing, Western Blot, Immunofluorescence, Migration, Immunohistochemical staining, Staining, MANN-WHITNEY, Quantitative RT-PCR

Exosomal miR-7108-3p regulated cancer cell growth in NSG mice. A - C Tumor size, volume changes, and weights of xenografts were analyzed in exosomal miR-7108-3p-treated group compared with controls. N = 5. D , E The PRF1 and Gzmb levels in the sera of exosomal miR-7108-3p-treated mice. F CD8 immunofluorescence analysis in xenografts. Bar = 125 μm. G Proposed model by which circZNF548 suppressed NSCLC proliferation by regulating JMY-p53 related genes and promoted the killing function of CTL through CD8. Data were shown as median (interquartile range), **p < 0.01; Student’s t-test or Mann–Whitney U test

Journal: BMC Biology

Article Title: m6A-modified circZNF548 regulates exosomal miR-7108-3p to activate CD3 + CD8 + T cells and suppress NSCLC growth by JMY

doi: 10.1186/s12915-025-02355-z

Figure Lengend Snippet: Exosomal miR-7108-3p regulated cancer cell growth in NSG mice. A - C Tumor size, volume changes, and weights of xenografts were analyzed in exosomal miR-7108-3p-treated group compared with controls. N = 5. D , E The PRF1 and Gzmb levels in the sera of exosomal miR-7108-3p-treated mice. F CD8 immunofluorescence analysis in xenografts. Bar = 125 μm. G Proposed model by which circZNF548 suppressed NSCLC proliferation by regulating JMY-p53 related genes and promoted the killing function of CTL through CD8. Data were shown as median (interquartile range), **p < 0.01; Student’s t-test or Mann–Whitney U test

Article Snippet: Membranes were incubated overnight at 4 °C with the following primary antibodies: rabbit anti-human GAPDH (1:3000, BS65656, Bioworld, MN, USA), rabbit anti-human P53 (1:1000, 60,283–2-lg, Proteintech, PA, USA), rabbit anti-human JMY (1:500, 25,098–1-AP, Proteintech), rabbit anti-human Bax (1:500, BS79706, Bioworld), rabbit anti-human Bcl2 (1:500, BZ16777, Bioworld), rabbit anti-human CD8a (1:500, 48,750–1, Signalway Antibody, MD, USA).

Techniques: Immunofluorescence, MANN-WHITNEY

Journal: Cell Reports Medicine

Article Title: UCHL1 is a potential molecular indicator and therapeutic target for neuroendocrine carcinomas

doi: 10.1016/j.xcrm.2023.101381

Figure Lengend Snippet:

Article Snippet: Rabbit anti- Human-p53 , Cell signaling , Cat#2527.

Techniques: Virus, Plasmid Preparation, Clinical Proteomics, Recombinant, Viability Assay, In Situ, Proximity Ligation Assay, Enzyme-linked Immunosorbent Assay, cDNA Synthesis, SYBR Green Assay, shRNA, Control, Ubiquitin Proteomics, Software