Aperçu des produits pour anti-RHOG (RHOG) Anticorps

Mouse (Murine) Ras Homolog Family Member G (RHOG) interaction partners

1. ELMO2-RhoG-ILK complex has a key role in integrin-independent stabilization of the microtubule network in differentiated keratinocytes.

2. RhoG is expressed and activated in platelets, plays an important role in GPVI-Fc receptor gamma-chain complex-mediated platelet activation, and is critical for thrombus formation in vivo.

3. RhoG protein regulates platelet granule secretion and thrombus formation in mice.

4. Examined the role of RhoG in the invasive behavior of glioblastoma cells; found that depletion of RhoG strongly inhibits activation of the Rac1 GTPase by both HGF and EGF; also RhoG contributes to the formation of lamellipodia and invadopodia.

5. several Rho family small GTPases activate PI3K by an indirect cooperative positive feedback that required a combination of Rac, CDC42, and RhoG small GTPase activities

6. Results indicate that RhoG promotes neural progenitor cell proliferation through PI3K in cortical development.

7. RhoG function is mediated by signals independent of Rac1 and Cdc42 activation and instead by direct utilization of a subset of common effectors

8. different biological properties of RhoG and Rac1 can be traced to specific amino acid variations in their switch I, beta2/beta3 hairpin, alpha5 helix, and C-terminal polybasic regions.

9. In RhoG deficient mice, the development of B and T lymphocytes was unaffected. However, there was an increase in the level of serum IgG1 and IgG2b as well as a mild increase of the humoral immune response to thymus-dependent antigens.

10. define RhoG as a critical component of G protein-coupled receptor-stimulated signaling cascades in murine neutrophils

11. Resutls show that the interaction with ELMO2 and RhoG is essential for the ability of ILK to induce front-rear cell polarity.

12. 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.

Human Ras Homolog Family Member G (RHOG) interaction partners

1. siRNA-mediated depletion of RHOG strongly inhibits tube formation in vascular endothelial cells (ECV cells), an effect reversed by transfecting dominant active constructs of CDC42 or RAC1 in the RHOG-depleted cells.

2. High RHOG expression is associated with lung adenocarcinoma.

3. RhoG and SGEF modulate the phosphorylation of paxillin, which plays a key role during invadopodia disassembly.

4. yrosine phosphorylation of SGEF suppresses its interaction with RhoG, the elevation of RhoG activity, and SGEF-mediated promotion of cell migration. We identified tyrosine 530 (Y530), which is located within the Dbl homology domain, as a major phosphorylation site of SGEF by Src, and Y530F mutation blocked the inhibitory effect of Src on SGEF

5. These results suggest that the levels of RhoG and RhoB GTPases and their negative regulator RhoGDI3 might be linked to the aggressiveness of the pancreatic cancerous cell lines. It is possible that RhoGDI3 could induce the downregulation of RhoG and RhoB.

6. These data suggest a novel link between Tiam1 and RhoG/ILK /ELMO2 pathway as upstream effectors of the Rac1-mediated phagocytic process in trabecular meshwork cells.

7. This study describes the regulation of EMT in RPE cells by TGF-beta1/miR-124/RHOG signaling and suggests that the supplement of miR-124 exogenously would be a valuable therapeutic approach for the prevention or treatment of proliferative vitreoretinopathy.

8. RhoG is expressed and activated in platelets, plays an important role in GPVI-Fc receptor gamma-chain complex-mediated platelet activation, and is critical for thrombus formation in vivo.

9. several Rho family small GTPases activate PI3K by an indirect cooperative positive feedback that required a combination of Rac, CDC42, and RhoG small GTPase activities

10. The invasive capacity of HPV transformed cells requires the hDlg-dependent enhancement of SGEF/RhoG activity.

11. The authors show that enteropathogenic Escherichia coli translocates EspH, which inactivates mammalian RhoGEFs and triggers cytotoxicity.

12. The activation of RhoG recruits its effector ELMO2 and a Rac GEF Dock4 to form a complex with EphA2 at the tips of cortactin-rich protrusions in migrating breast cancer cells.

13. RhoG function is mediated by signals independent of Rac1 and Cdc42 activation and instead by direct utilization of a subset of common effectors

14. we show a novel function for the small GTPase RhoG on the regulation of the interferon-gamma promoter and nuclear factor of activated T cells (NFAT) gene. RhoG also promotes T-cell spreading on fibronectin

15. C-terminal basic tail of RhoG specifically assists the recruitment of the TrioN-PH domain to specific membrane-bound phospholipids

16. Results suggest that RhoG contributes to the regulation of Rac1 activity in migrating cells.

17. RhoG is involved in caveolar trafficking. Such translocation is associated with changes in RhoG GDP/GTP levels and is highly dependent on lipid raft integrity and on the function of the GTPase dynamin2.

18. define RhoG as a critical component of G protein-coupled receptor-stimulated signaling cascades in murine neutrophils

19. Taken together, these results suggest that Dock4 plays an important role in the regulation of cell migration through activation of Rac1, and that RhoG is a key upstream regulator for Dock4.

20. RhoG protects cells from apoptosis caused by the loss of anchorage through a PI3K-dependent mechanism, independent of its activation of Rac1.