2008年6月15日 · We propose that loss of Net1 before EMT reduces basal RhoA activity and destabilizes basal microtubules, causing disruption of epithelial cell–BM interaction and subsequently, breakdown of the...

RhoA是具有GTP活性的小分子蛋白，在细胞分裂和增殖中起重要作用，能通过控制下游的效应因素，改变肌动蛋白的结构，调节细胞的生物学行为，包括细胞形态、增殖、凋亡、黏附和迁移 。RhoA对肿瘤的发病机制、浸润和肿瘤转移亦非常关键 。

AIBP 通过HIF1-a介导的EMT抑制肝细胞癌侵袭转移的研究; ING4/miR-940/Snail1途径 调控结直肠癌EMT和转移的作用及机制; MTDH 通过Wnt/β-catenin和Wnt/PCP通路协同介导舌癌细胞EMT促进侵袭转移的分子机制研究; 关于EMT

2023年3月22日 · Using genome-wide transcriptomic and proteomic profiling, we found that RHOJ regulates EMT-associated resistance to chemotherapy by enhancing the response to replicative stress and activating the...

2016年9月29日 · Transforming growth factor (TGF)-β-induced epithelial-mesenchymal transition (EMT) leads to the formation of ocular fibrotic pathologies, such as anterior subcapsular cataract and posterior capsule opacification. Remodeling of the actin cytoskeleton, mediated by the Rho family of GTPases, plays a key role in EMT.

Here we provide evidence that distinct cellular steps of EMT occur sequentially during gastrulation. Basement membrane (BM) breakdown is the first recognizable step and is controlled by loss of basally localized RhoA activity and its activator neuroepithelial-transforming-protein-1 …

2006年5月22日 · Here, we report that RhoC expression and activation are induced by the epithelial to mesenchymal transition (EMT) of colon carcinoma. Using LIM 1863 colon cancer cells, RhoC protein expression...

2018年1月12日 · Here, we studied the effects of RhoA/Rho-kinase signaling in AGEs-induced epithelial-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs), and evaluated morphological and molecular changes in a rat model of PD-related PF.

RhoA是Rho家族的重要成员，ROCK为RhoA的下游分子，有研究表明RhoA可能与TGF-β诱导的EMT发生有关。 本实验拟了解RhoA/ROCK通路是否参与了增生前列腺上皮细胞的EMT发生，为治疗BPH提供新的靶点。

2020年7月29日 · Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial‐mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up‐regulated the RhoA activity and expression of RhoA and ROCK1/2.