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Increased expression of bovine Rho GDIalpha (show GDI1 ELISA Kits) led to electrophysiological alterations that resulted in atrial arrhythmias and AV conduction abnormalities in transgenic mice, whereas ventricular contractile function was largely preserved.
that inhibition of Ca2 (show CA2 ELISA Kits)+ channel activity by overexpression of Rho GDI-alpha is mediated by inhibition of RhoA (show RHOA ELISA Kits) in cardiac myocytes
Rho GDP association inhibitor (GDI) alpha- mediated disruption of Rho GTPase (show RACGAP1 ELISA Kits) activity impairs lens fiber cell migration, elongation and survival.
Together, our results suggest a role for Ly-GDI (show ARHGDIB ELISA Kits) in the localized regulation of Rho GTPases in platelets and hypothesize a link between the PKC and Rho GTPase (show RACGAP1 ELISA Kits) signaling systems in platelet function.
MiR (show MLXIP ELISA Kits)-25 is activated by the WNT (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling pathway, and exerts its pro-metastatic function by directly inhibiting the Rho GDP dissociation inhibitor alpha (RhoGDI1). Downregulation of RhoGDI1 enhances expression of Snail (show SNAI1 ELISA Kits), thereby promoting EMT (show ITK ELISA Kits).
RIP2 (show ARHGEF28 ELISA Kits) and RhoGDI bind to p75(NTR (show NGFR ELISA Kits)) death domain at partially overlapping epitopes with over 100-fold difference in affinity, revealing the mechanism by which RIP2 (show ARHGEF28 ELISA Kits) recruitment displaces RhoGDI upon ligand binding.
Downregulation of RhoGDI could be a critical mechanism of breast tumor development, which may involve the hyperactivation of Rho GTPases and upregulation of COX-2 (show COX2 ELISA Kits) activity.
RHOGDI alpha acetylation interferes with Rho signaling, resulting in alteration of cellular filamentous actin.
the present study has identified loss of ARHGDIA contributed to the processes of hepatic tumorigenesis, in particular invasion and metastasis
new mechanistic insights into the understanding of essential role of SUMOylation at Lys (show LYZ ELISA Kits)-138 in RhoGDIalpha's biological function.
By directly targeting the Rho GDP dissociation inhibitor alpha (RhoGDI1) and activated leukocyte cell adhesion molecule (ALCAM (show ALCAM ELISA Kits)).
A significant trend was identified between loss of RhoGDI expression in hepatocellular carcinoma and worsening clinical prognosis.
Our findings suggest that RhoGDI overexpression is a predictor of distant metastasis and plays an important role in the progression of hepatocellular carcinoma
Integrin beta 8 and PTP-PEST (show PTPN12 ELISA Kits) form protein complexes at the leading edge of migrating cells and balance patterns of Rac1 and Cdc42 (show CDC42 ELISA Kits) signaling by controlling the subcellular localization and phosphorylation status of Rho GDP dissociation inhibitor 1.
RhoGDalpha controls ENaC expression and activity via Rac1.
the association of RhoGDIalpha with TROY (show TNFRSF19 ELISA Kits) contributed to TROY (show TNFRSF19 ELISA Kits)-dependent RhoA (show RHOA ELISA Kits) activation and neurite outgrowth inhibition after Nogo (show RTN4 ELISA Kits)-66 stimulation.
Data found that CCK (show CCK ELISA Kits)-induced PKCalpha (show PKCa ELISA Kits) phosphorylation on RhoGDI1 at Ser96 releases RhoA (show RHOA ELISA Kits) and Rac1 from RhoGDI1 to facilitate Rho GTPases signaling.
we demonstrated the regulation of targeting/accumulation of the RhoGDIalpha-Rac1 complex to phagosomes
how the beta cell utilizes RhoGDI for differential Cdc42 and Rac1 cycling
Inhibition of Rho family GTPases by Rho GDP dissociation inhibitor disrupts cardiac morphogenesis (show XIRP1 ELISA Kits) and inhibits cardiomyocyte proliferation.
analysis of inhibitory and shuttling functions of rhoGDI-3 (show ARHGDIG ELISA Kits) and rhoGDI-1
isoprenylcysteine carboxylmethyltransferase (show ICMT ELISA Kits) regulates Rac1 activity by controlling the interaction of Rac1 with RhoGDI through TNFA (show TNF ELISA Kits)
Aplysia Ras-related homologs (ARHs), also called Rho genes, belong to the RAS gene superfamily encoding small guanine nucleotide exchange (GTP/GDP) factors. The ARH proteins may be kept in the inactive, GDP-bound state by interaction with GDP dissociation inhibitors, such as ARHGDIA (Leffers et al., 1993
rho GDP-dissociation inhibitor 1
, Rho GDP dissociation inhibitor (GDI) alpha
, rho GDI 1
, rho-GDI alpha
, Rho GDI alpha