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Human Monoclonal ARHGDIA Primary Antibody pour ICC, FACS - ABIN969501
Ronneburg, Span, Kantelhardt, Dittmer, Schunke, Holzhausen, Sweep, Dittmer: Rho GDP dissociation inhibitor alpha expression correlates with the outcome of CMF treatment in invasive ductal breast cancer. dans International journal of oncology 2009
Show all 2 Pubmed References
Human Monoclonal ARHGDIA Primary Antibody pour ELISA, WB - ABIN559944
Liu, Huang, Xing, Xi, Zhuang, Yuan, Yang, Zhao: Comparative proteomic analysis on human L-02 liver cells treated with varying concentrations of trichloroethylene. dans Toxicology and industrial health 2008
Human Polyclonal ARHGDIA Primary Antibody pour IHC, ELISA - ABIN1531733
Xiao, Lin, Ke, Lin, Lin, Lin: 14-3-3τ promotes breast cancer invasion and metastasis by inhibiting RhoGDIα. dans Molecular and cellular biology 2014
connects the interaction between RhoGDI1 and ephrinB1 to the promotion of cancer cell behavior associated with tumor progression
Results indicate that protein phosphatase 1B (PPM1B) negatively regulates cancer cell motility and invasiveness through dephosphorylating Rho guanine nucleotide dissociation inhibitor 1 (RhoGDI1).
RhoGDIalpha is involved in the maintenance of glioma stem cells
analysis of the Kindlin-2-RhoGDIalpha-Rac1 signaling axis that is critical for regulation of podocyte structure and function in vivo
Data suggest that the interaction between PCBP2 and the 3'UTR of the ARHGDIA mRNA may induce a local change in RNA structure that favors subsequent binding of miR-151-5p and miR-16, thus leading to the suppression of ARHGDIA expression.
These molecular changes are indicative of long-term premature endothelial dysfunction and provide a mechanistic framework to the epidemiological data showing increased risk of cardiovascular disease at 0.5 Gy.
our results suggest that RhoGDIalpha regulate TRF1 and telomere length and may be novel prognostic biomarkers in colorectal cancer
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.
MiR-25 is activated by the WNT/beta-catenin 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, thereby promoting EMT.
RIP2 and RhoGDI bind to p75(NTR) death domain at partially overlapping epitopes with over 100-fold difference in affinity, revealing the mechanism by which RIP2 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 activity.
This study showed that ARHGD1A messenger RNA levels was significantly upregulated in subjects with schizophrenia in laminar and cellular samples.
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
Results identify a critical role for 14-3-3tau in promoting breast cancer metastasis, in part through binding to and inhibition of RhoGDIalpha, a negative regulator of Rho GTPases and a metastasis suppressor.
new mechanistic insights into the understanding of essential role of SUMOylation at Lys-138 in RhoGDIalpha's biological function.
By directly targeting the Rho GDP dissociation inhibitor alpha (RhoGDI1) and activated leukocyte cell adhesion molecule (ALCAM).
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
the association of RhoGDIalpha with TROY contributed to TROY-dependent RhoA activation and neurite outgrowth inhibition after Nogo-66 stimulation.
The effective GDI displacement that is observed is caused by inhibition of reformation of Rab:GDI complexes.
Increased expression of bovine Rho GDIalpha 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+ channel activity by overexpression of Rho GDI-alpha is mediated by inhibition of RhoA in cardiac myocytes
Rho GDP association inhibitor (GDI) alpha- mediated disruption of Rho GTPase activity impairs lens fiber cell migration, elongation and survival.
GDIalpha has a critical role in suppressing Rac1 activity in mature podocytes
The siRNA-mediated suppression of expression of alphaGDI especially affected vesicle dynamics.
Integrin beta 8 and PTP-PEST form protein complexes at the leading edge of migrating cells and balance patterns of Rac1 and Cdc42 signaling by controlling the subcellular localization and phosphorylation status of Rho GDP dissociation inhibitor 1.
RhoGDalpha controls ENaC expression and activity via Rac1.
Data found that CCK-induced PKCalpha phosphorylation on RhoGDI1 at Ser96 releases RhoA 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
Morphological analysis of Rho GDP Dissociation Inhibitor (-/-) renal mesangial cells reveals a decrease in cell spreading compared to wild-type cells and a decreased ability to proliferate and survive.
Inhibition of Rho family GTPases by Rho GDP dissociation inhibitor disrupts cardiac morphogenesis and inhibits cardiomyocyte proliferation.
analysis of inhibitory and shuttling functions of rhoGDI-3 and rhoGDI-1
isoprenylcysteine carboxylmethyltransferase regulates Rac1 activity by controlling the interaction of Rac1 with RhoGDI through TNFA
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.
RhoGDI-1 regulates lung microvessel endothelial barrier function by repressing RhoA activity.
Differential expression of RhoGDI-1, cofilin 1 and tropomyosin 2 in calpain-deficient fibroblasts compared with wild-type fibroblasts
liposomes supplemented with (PtdIns(3,4,5)P(3)) in conjunction with Rac, Trio, or Tiam1 and a non-hydrolyzable GTP analogue, cause dissociation of Rac1(GDP).RhoGDI complexes, GDP to GTP exchange on Rac1, and binding of Rac1(GTP) to the liposomes
In DGKzeta-deficient fibroblasts PAK1 phosphorylation and Rac1-RhoGDI dissociation were attenuated, leading to reduced Rac1 activation after platelet-derived growth factor stimulation.
Fibroblast growth factor 2-induced Rac1 activation depends on the suppression of RhoG by a previously uncharacterized ternary S4-synectin-RhoGDI1 protein complex and activation via PKCalpha.
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 GDI 1
, rho GDP-dissociation inhibitor 1
, rho-GDI alpha
, Rho GDP dissociation inhibitor (GDI) alpha
, Rho GDI alpha