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pan-tead #13295 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc pan-tead #13295 antibody
    Pan Tead #13295 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pan-tead #13295 antibody/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
    pan-tead #13295 antibody - by Bioz Stars, 2026-03
    90/100 stars

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    PITX2 acts as a potential partner TF of YAP in EACSCC. A and B, Dose–response curves of <t>VT104</t> in ONO2 cells examined in a proliferation assay ( n = 6; A ) and a clonogenic assay ( n = 3; B ). C, qPCR for YAP/TAZ-TEAD target genes upon treatment with VT104 (1 μmol/L) for 24 hours in ONO2 cells in vitro ( n = 3). D, YAP Co-IP experiment in ONO2 cells treated with VT104 (1 μmol/L) for 24 hours. E, Dose–response curves of VT104 in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 6). The IC 50 value for each group is shown. F, Proliferation assays in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 3). G, Transwell migration assays in ONO2 and FaDu upon siRNA-mediated knockdown against PITX2 ( n = 5). H, A volcano plot representing DEGs between PITX2-overexpressed and control ONO2 cells. Selected genes are highlighted as yellow dots. Genes with an adjusted P value < 0.01 and an absolute value of fold change >1.5 were considered significant. I, GO analysis for the DEGs upregulated in PITX2-overexpressed ONO2 cells compared with control cells in the Molecular Signature Database (MSigDB) Hallmark pathways. J, GSEA representing gene sets positively or negatively enriched in PITX2-overexpressed ONO2 cells compared with control cells in MSigDB Hallmark pathways. K, Western blots for the indicated proteins in PITX2-overexpressed and control ONO2 cells. L, Proliferation assays in PITX2-overexpressed and control ONO2 cells ( n = 5). M, Wound healing assays in PITX2-overexpressed and control ONO2 cells ( n = 3). N, Spheroid formation assays in PITX2-overexpressed and control ONO2 cells ( n = 6). O and P, Growth curves for PITX2-overexpressed or control ONO2 xenograft tumors ( O ) and bar plots for tumor weight at endpoint ( P ; n = 6). The image of tumors is also shown. Q, Representative images for HE staining as well as immunohistochemical staining for PITX2 and Ki67 in the xenograft tumors. Data represent mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    PITX2 acts as a potential partner TF of YAP in EACSCC. A and B, Dose–response curves of VT104 in ONO2 cells examined in a proliferation assay ( n = 6; A ) and a clonogenic assay ( n = 3; B ). C, qPCR for YAP/TAZ-TEAD target genes upon treatment with VT104 (1 μmol/L) for 24 hours in ONO2 cells in vitro ( n = 3). D, YAP Co-IP experiment in ONO2 cells treated with VT104 (1 μmol/L) for 24 hours. E, Dose–response curves of VT104 in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 6). The IC 50 value for each group is shown. F, Proliferation assays in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 3). G, Transwell migration assays in ONO2 and FaDu upon siRNA-mediated knockdown against PITX2 ( n = 5). H, A volcano plot representing DEGs between PITX2-overexpressed and control ONO2 cells. Selected genes are highlighted as yellow dots. Genes with an adjusted P value < 0.01 and an absolute value of fold change >1.5 were considered significant. I, GO analysis for the DEGs upregulated in PITX2-overexpressed ONO2 cells compared with control cells in the Molecular Signature Database (MSigDB) Hallmark pathways. J, GSEA representing gene sets positively or negatively enriched in PITX2-overexpressed ONO2 cells compared with control cells in MSigDB Hallmark pathways. K, Western blots for the indicated proteins in PITX2-overexpressed and control ONO2 cells. L, Proliferation assays in PITX2-overexpressed and control ONO2 cells ( n = 5). M, Wound healing assays in PITX2-overexpressed and control ONO2 cells ( n = 3). N, Spheroid formation assays in PITX2-overexpressed and control ONO2 cells ( n = 6). O and P, Growth curves for PITX2-overexpressed or control ONO2 xenograft tumors ( O ) and bar plots for tumor weight at endpoint ( P ; n = 6). The image of tumors is also shown. Q, Representative images for HE staining as well as immunohistochemical staining for PITX2 and Ki67 in the xenograft tumors. Data represent mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Research Communications

    Article Title: Aberrant Hippo-YAP/TEAD Signaling Drives Malignant Transcriptional Reprogramming in External Auditory Canal Squamous Cell Carcinoma

    doi: 10.1158/2767-9764.CRC-25-0626

    Figure Lengend Snippet: PITX2 acts as a potential partner TF of YAP in EACSCC. A and B, Dose–response curves of VT104 in ONO2 cells examined in a proliferation assay ( n = 6; A ) and a clonogenic assay ( n = 3; B ). C, qPCR for YAP/TAZ-TEAD target genes upon treatment with VT104 (1 μmol/L) for 24 hours in ONO2 cells in vitro ( n = 3). D, YAP Co-IP experiment in ONO2 cells treated with VT104 (1 μmol/L) for 24 hours. E, Dose–response curves of VT104 in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 6). The IC 50 value for each group is shown. F, Proliferation assays in ONO2 cells upon siRNA-mediated knockdown against PITX2 ( n = 3). G, Transwell migration assays in ONO2 and FaDu upon siRNA-mediated knockdown against PITX2 ( n = 5). H, A volcano plot representing DEGs between PITX2-overexpressed and control ONO2 cells. Selected genes are highlighted as yellow dots. Genes with an adjusted P value < 0.01 and an absolute value of fold change >1.5 were considered significant. I, GO analysis for the DEGs upregulated in PITX2-overexpressed ONO2 cells compared with control cells in the Molecular Signature Database (MSigDB) Hallmark pathways. J, GSEA representing gene sets positively or negatively enriched in PITX2-overexpressed ONO2 cells compared with control cells in MSigDB Hallmark pathways. K, Western blots for the indicated proteins in PITX2-overexpressed and control ONO2 cells. L, Proliferation assays in PITX2-overexpressed and control ONO2 cells ( n = 5). M, Wound healing assays in PITX2-overexpressed and control ONO2 cells ( n = 3). N, Spheroid formation assays in PITX2-overexpressed and control ONO2 cells ( n = 6). O and P, Growth curves for PITX2-overexpressed or control ONO2 xenograft tumors ( O ) and bar plots for tumor weight at endpoint ( P ; n = 6). The image of tumors is also shown. Q, Representative images for HE staining as well as immunohistochemical staining for PITX2 and Ki67 in the xenograft tumors. Data represent mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: Subsequently, cells were treated with VT104 TEAD inhibitor (#HY-134956, MedChemExpress) at concentrations ranging from 10 to 10,000 nmol/L for 6 days.

    Techniques: Proliferation Assay, Clonogenic Assay, In Vitro, Co-Immunoprecipitation Assay, Knockdown, Migration, Control, Western Blot, Staining, Immunohistochemical staining