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pyap1 ser109  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc pyap1 ser109
    TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, <t>pYAP1-Ser109,</t> TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.
    Pyap1 Ser109, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 394 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pyap1+ser109/pmc07281325-255-8-29?v=Cell+Signaling+Technology+Inc
    Average 96 stars, based on 394 article reviews
    pyap1 ser109 - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "The Hippo Pathway Transducers YAP1/TEAD Induce Acquired Resistance to Trastuzumab in HER2-Positive Breast Cancer"

    Article Title: The Hippo Pathway Transducers YAP1/TEAD Induce Acquired Resistance to Trastuzumab in HER2-Positive Breast Cancer

    Journal: Cancers

    doi: 10.3390/cancers12051108

    TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, pYAP1-Ser109, TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.
    Figure Legend Snippet: TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, pYAP1-Ser109, TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.

    Techniques Used: Isolation, Fractionation, Expressing, In Vitro

    Verteporfin-mediated regulation of the YAP1/TEAD signaling pathway restores sensitivity to antitumor activity of trastuzumab in BT-474.r2T cell line. ( A ) For in vitro experiments, 2.5 × 10 6 BT-474.r2T cells were seeded in 6-multiwell plates, and treatments were initiated after 96 h. For cell proliferation assays, BT-474.r2T cells left untreated (DMSO control), treated with 15 µg/mL trastuzumab, with 50 nM verteporfin, or with a combination of trastuzumab and verteporfin for 7 days. ( B ) WB of YAP1, pYAP1, TEAD1, and TEAD2 proteins were extracted after 48 h of 5 µM verteporfin treatment. Data are representative out of at least three independent replicates. ( C ) For the mRNA expression analyses of AREG , CTGF , CYR61 , and VEGFA , cells were left untreated (DMSO control) or treated with 5 µM verteporfin for 2 h. ( D ) Combination of trastuzumab and verteporfin decreases tumor proliferation and enhances apoptosis in mouse BT-474.r2T xenografts resistant to trastuzumab. Tumor growth and statistical analysis of control (10 mg/kg IgG ĸ), 10 mg/kg trastuzumab, 40 mg/kg with verteporfin, and combined trastuzumab with verteporfin groups of treatment.
    Figure Legend Snippet: Verteporfin-mediated regulation of the YAP1/TEAD signaling pathway restores sensitivity to antitumor activity of trastuzumab in BT-474.r2T cell line. ( A ) For in vitro experiments, 2.5 × 10 6 BT-474.r2T cells were seeded in 6-multiwell plates, and treatments were initiated after 96 h. For cell proliferation assays, BT-474.r2T cells left untreated (DMSO control), treated with 15 µg/mL trastuzumab, with 50 nM verteporfin, or with a combination of trastuzumab and verteporfin for 7 days. ( B ) WB of YAP1, pYAP1, TEAD1, and TEAD2 proteins were extracted after 48 h of 5 µM verteporfin treatment. Data are representative out of at least three independent replicates. ( C ) For the mRNA expression analyses of AREG , CTGF , CYR61 , and VEGFA , cells were left untreated (DMSO control) or treated with 5 µM verteporfin for 2 h. ( D ) Combination of trastuzumab and verteporfin decreases tumor proliferation and enhances apoptosis in mouse BT-474.r2T xenografts resistant to trastuzumab. Tumor growth and statistical analysis of control (10 mg/kg IgG ĸ), 10 mg/kg trastuzumab, 40 mg/kg with verteporfin, and combined trastuzumab with verteporfin groups of treatment.

    Techniques Used: Activity Assay, In Vitro, Control, Expressing



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    Cell Signaling Technology Inc pyap1 ser109
    TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, <t>pYAP1-Ser109,</t> TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.
    Pyap1 Ser109, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pyap1+ser109/pmc07281325-255-8-29?v=Cell+Signaling+Technology+Inc
    Average 96 stars, based on 1 article reviews
    pyap1 ser109 - by Bioz Stars, 2026-08
    96/100 stars
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    Image Search Results


    TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, pYAP1-Ser109, TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.

    Journal: Cancers

    Article Title: The Hippo Pathway Transducers YAP1/TEAD Induce Acquired Resistance to Trastuzumab in HER2-Positive Breast Cancer

    doi: 10.3390/cancers12051108

    Figure Lengend Snippet: TEAD1 and TEAD2 are highly expressed in trastuzumab-resistant BT-474.r2T cells and, together with YAP1, are upregulated in response to acquired trastuzumab resistance. 2.5E6 cells were seeded in 6-multiwell plates, and after 96 h of treatment, whole cell protein isolation, nuclear-cytoplasm protein fractionation, or RNA isolation were performed. ( A ) qPCR analysis of relative YAP1 , TAZ , TEAD1 , TEAD2 , TEAD3 , TEAD4 , AREG , CTGF , CYR61 , and VEGFA mRNA expression following in vitro generation of trastuzumab-resistant BT-474.r2T cells (*: p < 0.05, **: p < 0.01, ***: p < 0.001). ( B ) WB analysis of total YAP1, pYAP1-Ser109, TAZ, TEAD1, and TEAD2 expression in cells shown in ( A ). ( C ) WB analysis of total YAP, pYAP-Ser109, TAZ, TEAD1 and TEAD2 expression in the nuclear/cytosol extracts of cells shown in ( A ). Relative abundance levels of protein up- or downregulation were determined by densitometric analysis of the images.

    Article Snippet: Primary antibodies: TAZ (#4883), TEAD1 (#12292), YAP1 (#14074), pYAP1-Ser109 (#46931) pEGFR-Tyr1173 (#4407), EGFR (#4267), pHER2-TyrY1221/1222 (#2243), HER2 (#2242), pHER3-Tyr1289) (#4791), pHER4-Tyr1284 (#4757), HER4 (#4795), N-cadherin (#D4R1H), E-cadherin (#3195S) (1:1000), (Cell Signaling Technology, USA); lamin B1 (#ab16048), fibronectin (#ab2413) (1:1000), (Abcam); β-actin (1:10000) (#A5441), CTGF (#HPA031075) (1:250), GAPDH (#G8795) (1:10000), and TEAD2 (#SAB4503373), CD24 (#SAB4700624), occludin (#SAB4200593) (Sigma Aldrich); HER3 (#MA5-13053) (1:1000) (Invitrogen); vimentin (#550513BD) (1:1000) (Pharmigen).

    Techniques: Isolation, Fractionation, Expressing, In Vitro

    Verteporfin-mediated regulation of the YAP1/TEAD signaling pathway restores sensitivity to antitumor activity of trastuzumab in BT-474.r2T cell line. ( A ) For in vitro experiments, 2.5 × 10 6 BT-474.r2T cells were seeded in 6-multiwell plates, and treatments were initiated after 96 h. For cell proliferation assays, BT-474.r2T cells left untreated (DMSO control), treated with 15 µg/mL trastuzumab, with 50 nM verteporfin, or with a combination of trastuzumab and verteporfin for 7 days. ( B ) WB of YAP1, pYAP1, TEAD1, and TEAD2 proteins were extracted after 48 h of 5 µM verteporfin treatment. Data are representative out of at least three independent replicates. ( C ) For the mRNA expression analyses of AREG , CTGF , CYR61 , and VEGFA , cells were left untreated (DMSO control) or treated with 5 µM verteporfin for 2 h. ( D ) Combination of trastuzumab and verteporfin decreases tumor proliferation and enhances apoptosis in mouse BT-474.r2T xenografts resistant to trastuzumab. Tumor growth and statistical analysis of control (10 mg/kg IgG ĸ), 10 mg/kg trastuzumab, 40 mg/kg with verteporfin, and combined trastuzumab with verteporfin groups of treatment.

    Journal: Cancers

    Article Title: The Hippo Pathway Transducers YAP1/TEAD Induce Acquired Resistance to Trastuzumab in HER2-Positive Breast Cancer

    doi: 10.3390/cancers12051108

    Figure Lengend Snippet: Verteporfin-mediated regulation of the YAP1/TEAD signaling pathway restores sensitivity to antitumor activity of trastuzumab in BT-474.r2T cell line. ( A ) For in vitro experiments, 2.5 × 10 6 BT-474.r2T cells were seeded in 6-multiwell plates, and treatments were initiated after 96 h. For cell proliferation assays, BT-474.r2T cells left untreated (DMSO control), treated with 15 µg/mL trastuzumab, with 50 nM verteporfin, or with a combination of trastuzumab and verteporfin for 7 days. ( B ) WB of YAP1, pYAP1, TEAD1, and TEAD2 proteins were extracted after 48 h of 5 µM verteporfin treatment. Data are representative out of at least three independent replicates. ( C ) For the mRNA expression analyses of AREG , CTGF , CYR61 , and VEGFA , cells were left untreated (DMSO control) or treated with 5 µM verteporfin for 2 h. ( D ) Combination of trastuzumab and verteporfin decreases tumor proliferation and enhances apoptosis in mouse BT-474.r2T xenografts resistant to trastuzumab. Tumor growth and statistical analysis of control (10 mg/kg IgG ĸ), 10 mg/kg trastuzumab, 40 mg/kg with verteporfin, and combined trastuzumab with verteporfin groups of treatment.

    Article Snippet: Primary antibodies: TAZ (#4883), TEAD1 (#12292), YAP1 (#14074), pYAP1-Ser109 (#46931) pEGFR-Tyr1173 (#4407), EGFR (#4267), pHER2-TyrY1221/1222 (#2243), HER2 (#2242), pHER3-Tyr1289) (#4791), pHER4-Tyr1284 (#4757), HER4 (#4795), N-cadherin (#D4R1H), E-cadherin (#3195S) (1:1000), (Cell Signaling Technology, USA); lamin B1 (#ab16048), fibronectin (#ab2413) (1:1000), (Abcam); β-actin (1:10000) (#A5441), CTGF (#HPA031075) (1:250), GAPDH (#G8795) (1:10000), and TEAD2 (#SAB4503373), CD24 (#SAB4700624), occludin (#SAB4200593) (Sigma Aldrich); HER3 (#MA5-13053) (1:1000) (Invitrogen); vimentin (#550513BD) (1:1000) (Pharmigen).

    Techniques: Activity Assay, In Vitro, Control, Expressing