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YAP-TEAD Inhibitor 1 (Peptide 17)

目录号 : GC26088

YAP-TEAD Inhibitor 1 (Peptide 17) is a YAP-TEAD protein-protein interaction inhibitor which has potential usage in treatment of YAP-involved cancers with IC50 of 25 nM.

YAP-TEAD Inhibitor 1 (Peptide 17) Chemical Structure

Cas No.:1659305-78-8

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1mg
¥1,129.00
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产品描述

YAP-TEAD Inhibitor 1 (Peptide 17) is a YAP-TEAD protein-protein interaction inhibitor which has potential usage in treatment of YAP-involved cancers with IC50 of 25 nM.

The engineered peptide significantly improves the potency in disrupting YAP-TEAD interaction in vitro[1]. This 17mer peptide demonstrates a single-digit micromolar affinity to TEAD1[2].

[1] Zhang Z, et al. ACS Med Chem Lett. 2014, 5(9):993-998. [2] Zhou Z, et al. FASEB J. 2015, 29(2):724-732.

Chemical Properties

Cas No. 1659305-78-8 SDF Download SDF
分子式 C93H144ClN23O21S2 分子量 2019.86
溶解度 Water: 40 mg/mL (19.80 mM) 储存条件 Store at -20°C
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1 mM 0.4951 mL 2.4754 mL 4.9508 mL
5 mM 0.099 mL 0.4951 mL 0.9902 mL
10 mM 0.0495 mL 0.2475 mL 0.4951 mL
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Research Update

FSH Regulates YAP-TEAD Transcriptional Activity in Bovine Granulosa Cells to Allow the Future Dominant Follicle to Exert Its Augmented Estrogenic Capacity

Int J Mol Sci 2022 Nov 16;23(22):14160.PMID:36430640DOI:10.3390/ijms232214160.

The molecular mechanisms that drive the granulosa cells' (GC) differentiation into a more estrogenic phenotype during follicular divergence and establishment of follicle dominance have not been completely elucidated. The main Hippo signaling effector, YAP, has, however, emerged as a potential key player to explain such complex processes. Studies using rat and bovine GC demonstrate that, in conditions where the expression of the classic YAP-TEAD target gene tissue growth factor (CTGF) is augmented, CYP19A1 expression and activity and, consequently, estradiol (E2) secretion are reduced. These findings led us to hypothesize that, during ovarian follicular divergence in cattle, FSH downregulates YAP-TEAD-dependent transcriptional activity in GC to allow the future dominant follicle to exert its augmented estrogenic capacity. To address this, we performed a series of experiments employing distinct bovine models. Our in vitro and ex vivo experiments indicated that indeed FSH downregulates, in a concentration-dependent manner, mRNA levels not only for CTGF but also for the other classic YAP-TEAD transcriptional target genes ANKRD1 and CYR61 by a mechanism that involves increased YAP phosphorylation. To better elucidate the functional importance of such FSH-induced YAP activity regulation, we then cultured GC in the presence of verteporfin (VP) or Peptide 17 (P17), two pharmacological inhibitors known to interfere with YAP binding to TEADs. The results showed that both VP and P17 increased CYP19A1 basal mRNA levels in a concentration-dependent manner. Most interestingly, by using GC samples obtained in vivo from dominant vs. subordinate follicles, we found that mRNA levels for CTGF, CYR61, and ANKRD1 are higher in subordinate follicles following the follicular divergence. Taken together, our novel results demonstrate that YAP transcriptional activity is regulated in bovine granulosa cells to allow the increased estrogenic capacity of the selected dominant follicle.

TM4SF1 facilitates non-small cell lung cancer progression through regulating YAP-TEAD pathway

Eur Rev Med Pharmacol Sci 2020 Feb;24(4):1829-1840.PMID:32141552DOI:10.26355/eurrev_202002_20361.

Objective: Transmembrane-4-L- Six-Family-1 (TM4SF1) has been found involved in the development and progression of tumor. This study aims to investigate the effect of TM4SF1 on the proliferation, migration, and invasion of non-small cell lung cancer (NSCLC) and reveal its underlying mechanisms. Materials and methods: qRT-PCR, immunohistochemical analysis, and Western blot were used to evaluate the expression of TM4SF1 in human NSCLC tissues and cells. Cell proliferation was measured by CCK-8 and colony formation assay. Cell apoptosis was evaluated by flow cytometry assay. Cell migration and invasion were detected by wound healing and transwell assays. Co-immunoprecipitation (Co-IP) assay was used to examine the interactions between proteins. Expression levels of related proteins were determined by Western blot. For in vivo experiment, xenograft tumor models were used. Results: TM4SF1 was upregulated in NSCLC tissues and cell lines and closely correlated to survival time, tumor size, lymph node metastasis, distant metastasis, and clinical stage. Gain-of function and loss-of function experiments demonstrated the oncogenic effect of TM4SF1 on NSCLC cell proliferation, apoptosis, migration, and invasion. Notably, mechanism studies showed that TM4SF1 regulated the interaction between YAP and TEAD and the level of downstream target genes. Besides, sh-YAP or Peptide 17 treatment (YAP-TEAD protein-protein interaction inhibitor) reversed the effect of TM4SF1 on NSCLC cells. The in vivo research suggested that the knockdown of TM4SF1 inhibited the growth of xenograft tumor of NSCLC. Conclusions: This is the first evidence demonstrating that TM4SF1 could promote proliferation, migration, and invasion in NSCLC, at least partially through a potential YAP-TEAD signaling pathway-dependent mechanism. This study might provide a potential therapeutic target for the treatment of NSCLC.