跳转至内容

Dear Customer:

The current international situation is complex and volatile, and uncertain tariff policies may potentially impact our product prices. Given these uncertainties, we value your understanding regarding order-related matters.

If you decide to place an order during this period, we reserve the right to adjust the price based on the evolving situation. We understand that market changes may cause inconvenience. We will negotiate with you if there’s a significant price fluctuation due to tariff policy changes before the order’s actual delivery, and in such cases we may adjust or cancel the order as necessary.

We are planning system maintenance between Friday, Apr 11 at 9:00 PM CDT and Saturday, Apr 12 at 9:00 AM CDT. This will impact both web and offline transactions, including online orders, quotes, price and availability checks, and order status inquiries. We apologize for any inconvenience.

Merck
CN
  • DLC1 is a direct target of activated YAP/TAZ that drives collective migration and sprouting angiogenesis.

DLC1 is a direct target of activated YAP/TAZ that drives collective migration and sprouting angiogenesis.

Journal of cell science (2020-01-23)
Miesje van der Stoel, Lilian Schimmel, Kalim Nawaz, Anne-Marieke van Stalborch, Annett de Haan, Alexandra Klaus-Bergmann, Erik T Valent, Duco S Koenis, Geerten P van Nieuw Amerongen, Carlie J de Vries, Vivian de Waard, Martijn Gloerich, Jaap D van Buul, Stephan Huveneers
摘要

Endothelial YAP/TAZ (YAP is also known as YAP1, and TAZ as WWTR1) signaling is crucial for sprouting angiogenesis and vascular homeostasis. However, the underlying molecular mechanisms that explain how YAP/TAZ control the vasculature remain unclear. This study reveals that the focal adhesion protein deleted-in-liver-cancer 1 (DLC1) is a direct transcriptional target of the activated YAP/TAZ-TEAD complex. We find that substrate stiffening and VEGF stimuli promote expression of DLC1 in endothelial cells. In turn, DLC1 expression levels are YAP and TAZ dependent, and constitutive activation of YAP is sufficient to drive DLC1 expression. DLC1 is needed to limit F-actin fiber formation, integrin-based focal adhesion lifetime and integrin-mediated traction forces. Depletion of endothelial DLC1 strongly perturbs cell polarization in directed collective migration and inhibits the formation of angiogenic sprouts. Importantly, ectopic expression of DLC1 is sufficient to restore migration and angiogenic sprouting in YAP-depleted cells. Together, these findings point towards a crucial and prominent role for DLC1 in YAP/TAZ-driven endothelial adhesion remodeling and collective migration during angiogenesis.This article has an associated First Person interview with the first author of the paper.

材料
货号
品牌
产品描述

Sigma-Aldrich
黏着斑蛋白单克隆抗体 小鼠抗, clone hVIN-1, ascites fluid
登录查看公司和协议定价
货号包装规格是否有货价格数量
5 mg
预计发货时间 2025年4月14日
详情...
¥3,881.13
Supelco
甜蜜素, analytical standard
登录查看公司和协议定价
货号包装规格是否有货价格数量
5 mg
预计发货时间 2025年4月14日
详情...
¥3,881.13
Sigma-Aldrich
抗-WWTR1 兔抗, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
登录查看公司和协议定价
货号包装规格是否有货价格数量
5 mg
预计发货时间 2025年4月14日
详情...
¥3,881.13
Sigma-Aldrich
3-(联苯-4-基)-5-(4-叔丁基苯基)-4-苯基-4H-1,2,4-三唑, 97%
登录查看公司和协议定价
货号包装规格是否有货价格数量
5 mg
预计发货时间 2025年4月14日
详情...
¥3,881.13