rho-Specific Guanine Nucleotide Dissociation Inhibitors

08/01/2017 - "Results from the present study indicate that RhoGDI dysregulation is a frequent event in human HCC, and that it promotes cancer progression by stimulating cell migration and invasion. "
10/20/2015 - "Here we report that loss of RhoGDI significantly accelerated xenograft tumor growth of MDA-MB-231 cells in animal models. "
04/20/2012 - "We further demonstrated that RhoGDI SUMOylation at Lys-138 was crucial for inhibiting actin polymerization and cytoskeleton formation as well as cancer cell motility. "
11/01/2010 - "Rho GDI is frequently overexpressed in many human cancers. "
11/15/2007 - "This may be the net effect of two opposing activities of Rho-GDI beta, one that suppresses tumor progression by inhibiting migration and the other that stimulates it by enhancing Cox-2 expression."

11/15/2007 - "Our data suggest that the expression of Rho-GDI beta in breast cancer is neither beneficial nor disadvantageous to the patient. "
11/15/2007 - "Furthermore, in primary breast cancer, Rho-GDI beta is coexpressed with Ets1. "
11/15/2007 - "Here, we show that, in breast cancer cells, Ets1 regulates Rho-GDI beta expression and binds to the upstream region of the Rho-GDI beta gene. "
12/15/2003 - "This suggests that the expression of Rhos and Rho-GDIs in breast cancer is unbalanced and that this disturbance has clinical significance in breast cancer."
10/20/2015 - "We found that RhoGDI expression is higher in the early stages of breast cancer followed by a significant decrease in malignant tumors and metastatic lesions (p < 0.01). "

01/31/2014 - "Our findings suggest that RhoGDI overexpression is a predictor of distant metastasis and plays an important role in the progression of HCC. "
01/31/2014 - "RhoGDI overexpression correlated with postoperative distant metastasis. "
01/15/2016 - "Therefore, previous studies reporting that a RhoGDI(Y153E) mutant suppresses the metastasis of human bladder cancer cells must be reinvestigated in light of artificial interaction of this point mutant with FLNA. "
01/31/2014 - "Overexpression of RhoGDI, a novel predictor of distant metastasis, promotes cell proliferation and migration in hepatocellular carcinoma."
04/20/2012 - "The physiological regulation of RhoGDI SUMOylation by the RING domain of XIAP may account for modulation of cancer cell invasion and metastasis by XIAP."

01/15/2016 - "Therefore, previous studies reporting that a RhoGDI(Y153E) mutant suppresses the metastasis of human bladder cancer cells must be reinvestigated in light of artificial interaction of this point mutant with FLNA. "
05/01/2010 - "Using examples of RhoGDI-mediated signaling and expression patterns in endothelial cells as well as pancreatic, breast, and bladder cancer, the multitude of potential cancer therapeutic targets presented by a better understanding of their function is illustrated. "
11/01/2019 - "Emmprin, survivin, HMGA2, MTA1, RhoGDI, PEG10, TGM2, and TLN1 expressions were analyzed in paraffin-embedded bladder cancer tissue samples of 106 patients who underwent adjuvant or salvage cisplatin-based chemotherapy by using immunohistochemistry. "

01/01/2019 - "Together, the results of this study reveal a novel mechanism by which Ang II regulates RhoGDI stability by SUMOylation and ubiquitination via AT1 receptor activation and thus affects VSMC proliferation and vascular remodeling."
07/01/2019 - "These data suggested that ROCK inhibitors alleviate myofibroblast transdifferentiation and vascular remodeling by decreasing TGFβ1-mediated expression of RhoGDI."
07/01/2019 - "ROCK inhibitors alleviate myofibroblast transdifferentiation and vascular remodeling via decreasing TGFβ1-mediated RhoGDI expression."
01/01/2019 - "RhoGDI stability is regulated by SUMOylation and ubiquitination via the AT1 receptor and participates in Ang II-induced smooth muscle proliferation and vascular remodeling."
01/01/2019 - "We investigated the function of RhoGDI in angiotensin II (Ang II)-induced vascular remodeling in cultured human aortic vascular smooth muscle cells (HA-VSMCs) and in an Ang II-infusion vascular remodeling mouse model. "