yap1 ser109 Search Results


anti phospho yap1  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc anti phospho yap1
Anti Phospho Yap1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti phospho yap1/product/Cell Signaling Technology Inc
Average 94 stars, based on 1 article reviews
anti phospho yap1 - by Bioz Stars, 2026-03
94/100 stars
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pyap1 ser109  (Cell Signaling Technology Inc)
96
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/result/pyap1 ser109/product/Cell Signaling Technology Inc
Average 96 stars, based on 1 article reviews
pyap1 ser109 - by Bioz Stars, 2026-03
96/100 stars
  Buy from Supplier

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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