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anti-Human ARHGDIB Antibodies:
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Human Polyclonal ARHGDIB Primary Antibody for BI, WB - ABIN967542
Chong, Traynor-Kaplan, Bokoch, Schwartz: The small GTP-binding protein Rho regulates a phosphatidylinositol 4-phosphate 5-kinase in mammalian cells. in Cell 1994
Show all 4 references for ABIN967542
Human Polyclonal ARHGDIB Primary Antibody for IHC (p), WB - ABIN657665
Niu, Li, Xu, He: Expression profile of RhoGDI2 in lung cancers and role of RhoGDI2 in lung cancer metastasis. in Oncology reports 2010
Show all 3 references for ABIN657665
Human Polyclonal ARHGDIB Primary Antibody for ELISA, WB - ABIN559945
Zhao, Chang, Li, Shedden, Thomas, Misek, Manoharan, Giordano, Beer, Lubman: Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping. in Molecular & cellular proteomics : MCP 2007
Show all 2 references for ABIN559945
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 Antibodies) and is not a bona-fide interaction.
Results show that RhoGDI2 suppresses bladder cancer metastatic colonization via negative regulation of RhoC (show RHOC Antibodies) activity, providing a rationale for the development of therapeutics that target RhoC (show RHOC Antibodies) 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 Antibodies)/Akt (show AKT1 Antibodies) pathway and MMP-9 (show MMP9 Antibodies).
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 Antibodies) 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 Antibodies) 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 Antibodies) activity.
these results indicate that RhoGDIbeta functions as a novel BMP4 (show BMP4 Antibodies) signaling target that regulates adipogenesis and myogensis.
Raptor (show RPTOR Antibodies) siRNA suppressed the effects of GM3 (show GRM6 Antibodies) on Ly-GDI expression and Akt (show AKT1 Antibodies) phosphorylation at Thr (show TRH Antibodies)(308) , suggesting GM3 (show GRM6 Antibodies) signals to be transduced to mTOR (show FRAP1 Antibodies)-Raptor (show RPTOR Antibodies) and Akt (show AKT1 Antibodies)-Thr (show TRH Antibodies)(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 Antibodies) 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