YAP-TEAD Inhibitor 1 (Peptide 17)
目录号 : GC26088YAP-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.
Cas No.:1659305-78-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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.
| 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 |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 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 |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
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.