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Binders to RhoGDI2 as a potential anti-cancer target have been first reported, and their weak interactions were depicted using NMR spectroscopy.
Together, our results suggest a role for Ly-GDI in the localized regulation of Rho GTPases in platelets and hypothesize a link between the PKC (show PRRT2 Proteins) and Rho GTPase (show RACGAP1 Proteins) signaling systems in platelet function.
Delta19RhoGDIbeta has an apoptosisindependent role in the phorbol 12myristate 13acetate induced differentiation of THP1 cells to macrophages.
The caspase-3 (show CASP3 Proteins)-cleaved RhoGDIbeta is a possible determinant to promote cancer spreading.
Our interpretation of these contradictions is that truncation and/or mutation of RhoGDI2 perturbs its conformation to expose a site that adventitiously binds FLNA (show FLNA Proteins) and is not a bona-fide interaction.
Results show that RhoGDI2 suppresses bladder cancer metastatic colonization via negative regulation of RhoC (show RHOC Proteins) activity, providing a rationale for the development of therapeutics that target RhoC (show RHOC Proteins) signaling.
These findings indicate that RhoGDI2 repressed the activity of Rac1 and may be involved in the rearrangement of cytoskeleton in lung cancer cells.
Short hairpin RNA-mediated knockdown of RhoGDI2 induces the invasion and migration of lung cancer due to cross-talk with the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) pathway and MMP-9 (show MMP9 Proteins).
RhoGDI2 overexpression is associated with tumor growth, metastasis, and chemoresistance in gastric cancer.
Depletion of RhoGDI2 expression inhibits the ability of invasion and migration in pancreatic carcinoma.
Ly-GDI is a critical regulator of inflammatory injury after deposition of IgG immune complexes and that it negatively regulates the lung NF-kappaB (show NFKB1 Proteins) activity.
these results indicate that RhoGDIbeta functions as a novel BMP4 (show BMP4 Proteins) signaling target that regulates adipogenesis and myogensis.
Rictor regulates cell migration by suppressing RhoGDI2.
Raptor (show RPTOR Proteins) siRNA suppressed the effects of GM3 (show GRM6 Proteins) on Ly-GDI expression and Akt (show AKT1 Proteins) phosphorylation at Thr (show TRH Proteins)(308) , suggesting GM3 (show GRM6 Proteins) signals to be transduced to mTOR (show FRAP1 Proteins)-Raptor (show RPTOR Proteins) and Akt (show AKT1 Proteins)-Thr (show TRH Proteins)(308) , leading to Ly-GDI stimulation
Impaired interaction of RhoGDIbeta with Rac1 isoprenyl groups possibly makes RhoGDIbeta function as a positive regulator for Rac1 during metastasis.
Rho GDIalpha (show GDI1 Proteins) and Rho GDIbeta play synergistic roles in lymphocyte migration and development by modulating activation cycle of the Rho proteins in a lymphoid organ-specific manner.
Members of the Rho (or ARH) protein family (see MIM 165390) and other Ras-related small GTP-binding proteins (see MIM 179520) are involved in diverse cellular events, including cell signaling, proliferation, cytoskeletal organization, and secretion. The GTP-binding proteins are active only in the GTP-bound state. At least 3 classes of proteins tightly regulate cycling between the GTP-bound and GDP-bound states: GTPase-activating proteins (GAPs), guanine nucleotide-releasing factors (GRFs), and GDP-dissociation inhibitors (GDIs). The GDIs, including ARHGDIB, decrease the rate of GDP dissociation from Ras-like GTPases (summary by Scherle et al., 1993
rho GDP-dissociation inhibitor 2
, Rho GDP dissociation inhibitor (GDI) beta
, D4-GDP-dissociation inhibitor
, rho GDI 2
, rho-GDI beta
, Rho GDI 2