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RhoGDIbeta overexpression led to downregulation of miR-200c, whereas miR-200c was able directly to target 3'-UTR of jnk2mRNA and attenuated JNK2 protein translation, which resulted in attenuation of Sp1mRNA and protein expression in turn, inhibiting Sp1-dependent MMP-2 transcription.
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 and Rho GTPase 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-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 and is not a bona-fide interaction.
Results show that RhoGDI2 suppresses bladder cancer metastatic colonization via negative regulation of RhoC activity, providing a rationale for the development of therapeutics that target RhoC 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/Akt pathway and MMP-9.
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.
RhoGDI2 inhibits trophoblast cell migration, and this function may involve suppression of RAC1 activation.
14-3-3sigma is a RhoGDI2-regulated gene that appears to be important for suppressing the chemoresistance of gastric cancer cells.
These results suggest that RhoGDIbeta has mitotic functions, including regulation of cytokinesis and bipolar spindle formation
Rictor regulates cell migration by suppressing RhoGDI2.
RhoGDI2 becomes rapidly phosphorylated at Ser31 in response to phorbol 12-myristate 13-acetate stimulation. Conventional type PKCalpha is responsible for this phosphorylation.
Expression of ARHGDIB variants 6a, 6b, and 6c appears to be restricted to cancer cells and normal placental tissue, suggesting that these variants possess cancer-specific functions.
The ARHGDIB is a lymphoid-specific intrinsic negative regulator of HIV-1 replication that acts by simultaneously inhibiting RhoA and Rac1 functions.
Results suggest that D4-GDI may function as a biphasic regulator of breast cancer progression and metastasis.
We delineate the mechanism by which RhoGDI2 promotes gastric cancer cell invasion and chemoresistance. In total, 47 differential protein spots were identified; 33 were upregulated, and 14 were downregulated by RhoGDI2 overexpression.
Ly-GDI is a critical regulator of inflammatory injury after deposition of IgG immune complexes and that it negatively regulates the lung NF-kappaB activity.
these results indicate that RhoGDIbeta functions as a novel BMP4 signaling target that regulates adipogenesis and myogensis.
Raptor siRNA suppressed the effects of GM3 on Ly-GDI expression and Akt phosphorylation at Thr(308) , suggesting GM3 signals to be transduced to mTOR-Raptor and Akt-Thr(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 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