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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 ELISA Kits) and is not a bona-fide interaction.
Results show that RhoGDI2 suppresses bladder cancer metastatic colonization via negative regulation of RhoC (show RHOC ELISA Kits) activity, providing a rationale for the development of therapeutics that target RhoC (show RHOC ELISA Kits) 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 ELISA Kits)/Akt (show AKT1 ELISA Kits) pathway and MMP-9 (show MMP9 ELISA Kits).
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.
Rictor (show RICTOR ELISA Kits) regulates cell migration by suppressing RhoGDI2.
RhoGDI2 becomes rapidly phosphorylated at Ser31 in response to phorbol 12-myristate 13-acetate stimulation. Conventional type PKCalpha (show PKCa ELISA Kits) is responsible for this phosphorylation.
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 ELISA Kits) activity.
these results indicate that RhoGDIbeta functions as a novel BMP4 (show BMP4 ELISA Kits) signaling target that regulates adipogenesis and myogensis.
Raptor (show RPTOR ELISA Kits) siRNA suppressed the effects of GM3 (show GRM6 ELISA Kits) on Ly-GDI expression and Akt (show AKT1 ELISA Kits) phosphorylation at Thr (show TRH ELISA Kits)(308) , suggesting GM3 (show GRM6 ELISA Kits) signals to be transduced to mTOR (show FRAP1 ELISA Kits)-Raptor (show RPTOR ELISA Kits) and Akt (show AKT1 ELISA Kits)-Thr (show TRH ELISA Kits)(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 ELISA Kits) 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