在香港中文大学生物医学学院、香港城市大学生物医学系课题团队的一项研究中，将抗精神病药物硫利达嗪（Thioridazine）确定为一种有效的YAP抑制剂。 在体内和体外实验中，硫利达嗪抑制了紊乱血流诱导的内皮炎症反应，此外，硫利达嗪的给药在两种小鼠动脉粥样硬化模型中发挥了抗动脉粥样硬化作用。 该研究还为硫利达嗪抑制RhoA调节YAP活性的潜在机制提供了新的见解。 这项研究开辟了将硫利达嗪重新用于干预动脉粥样硬化疾病的可能性。

2024年1月15日 · Mechanistically, direct oxidation of RhoA by mitochondrial superoxide was responsible for PP2A-mediated YAP/TAZ dephosphorylation providing a novel physiological input for the Hippo pathway....

2021年11月3日 · 接着，作者探究了星形胶质细胞中RhoA诱导的肌动蛋白致密抑制星形胶质细胞反应性的机制，发现由肌动蛋白细胞骨架调控的关键因子YAP (yes-associatedprotein,Yes相关蛋白)参与其中。

2021年9月6日 · Mechanistically, RhoAG14V induced the expression and nuclear translocation of YAP/TAZ to produce CTGF. Moreover, inhibition of ROCK or YAP decreased the expression of Collagen I and α-SMA proteins induced by DEX or RhoAG14V in HTM cells.

2017年5月15日 · Here we unveil the molecular mechanism by which cell spreading and RhoA GTPase activity control FA formation through YAP to stabilize the anchorage of the actin cytoskeleton to the cell...

2021年9月6日 · Schematic diagram of RhoA/ROCK and YAP/TAZ mediated fibrotic activity in DEX-treated HTM cells. RhoA/ROCK activated by DEX induces nuclear translocation of YAP/TAZ, which leads to an increase of Collagen I, myofibroblast biomarker α-SMA, and CTGF. Aberrant ECM accumulation and remodeling may increase the elastic modulus of HTM cells.

As crucial downstream effectors of Hippo pathway, YAP is inhibited by Lats1/2 through phosphorylation. However, upstream signals that regulate the Hippo pathway have been still poorly understood. Here, we found that knockdown of CD44 reduced YAP expression and nuclear localization, but nearly had no effect on its upstream effectors, Mst1 and Lats1.

2014年11月1日 · RhoA was involved in the regulation of YAP by CD44. Our study provides new sights into the regulatory mechanisms of Hippo-YAP pathway. The Hippo pathway plays an important role in both physical and pathogenesis processes. As crucial downstream effectors of Hippo pathway, YAP is inhibited by Lats1/2 through phosphorylation.

富血小板血浆释放的外泌体可能通过激活PI3K/Akt和Erk信号通路来促进内皮细胞增殖。同时，通过激活Rho/YAP信号通路诱导再上皮化，从而促进糖尿病大鼠慢性创面的愈合。

2024年2月22日 · 在香港中文大学生物医学学院、香港城市大学生物医学系课题团队的一项研究中，将抗精神病药物硫利达嗪（Thioridazine）确定为一种有效的YAP抑制剂。 在体内和体外实验中，硫利达嗪抑制了紊乱血流诱导的内皮炎症反应，此外，硫利达嗪的给药在两种小鼠动脉粥样硬化模型中发挥了抗动脉粥样硬化作用。 该研究还为硫利达嗪抑制RhoA调节YAP活性的潜在机制提供了新的见解。 这项研究开辟了将硫利达嗪重新用于干预动脉粥样硬化疾病的可能性。