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The results of this study show that Rac3 have a roles in the formation of GABAergic circuits, as highlighted by the differential effects of their deletion on the late maturation of specific populations.
This study showed that in the absence of both Rac1 and rac3, the embryonic migration of medial ganglionic eminence-derived interneurons is further impaired.
This study demonistrated that Rac1 and rac3 GTPases control synergistically the development of cortical and hippocampal GABAergic interneurons in mice.
Rac1b forms a complex with NADPH oxidase (show NOX1 ELISA Kits) and promotes the production of reactive oxygen species, expression of Snail (show SNAI1 ELISA Kits), and activation of the epithelial-mesenchymal transition program.
Activation of epithelial-mesenchymal transition by MMP-induced expression of Rac1b gave rise to lung adenocarcinoma.
Rac1 and Rac3 redundantly regulate many aspects of inner ear morphogenesis, including cell adhesion, cell proliferation, cell death and cell movements.
Rac1 and Rac3 GTPases participate in the normal development of hilar mossy cells.
results support a role for neuronal Rac1 and Rac3 in dictating proper lymphoid organ development, and suggest the existence of lymphoid-extrinsic mechanisms linking neural defects to the loss of immune-competence
These defects result from increased RhoA/ROCK/myosin II activity and blockade of Rac1 signaling.
The 19-amino acid insertion in the tumor-associated splice isoform Rac1b confers specific binding to p120 catenin (show CTNND1 ELISA Kits)
RAC3 is an inhibitor of senescence whose downregulation in aged individuals could be probably a tumor suppressor mechanism.
Efficient silencing of Rac3 strongly inhibited A549 cell proliferation.
Collectively these data unveil that FBXL19 (show FBXL19 ELISA Kits) functions as an antagonist of Rac3 by regulating its stability and regulates the TGFbeta1 (show TGFB1 ELISA Kits)-induced E-cadherin (show CDH1 ELISA Kits) down-regulation.
Report role of Rac3 in breast cancer aggressiveness and show the potential usefulness of Rac3 depletion in breast cancer therapy.
RAC3 bound tightly to the ARE enhancer region of the HO-1 (show HMOX1 ELISA Kits) promoter via Nrf2 (show GABPA ELISA Kits) binding.
Hypoxia inhibits the RAC3 gene expression leading to the autophagy process, allowing tumor cells to survive until angiogenesis occurs
Rac3 GTPase (show RACGAP1 ELISA Kits) has a role in the regulation of autophagy
RAC3 is a novel ERalpha (show ESR1 ELISA Kits) co-activator that promotes cell migration and has prognostic value for ERalpha (show ESR1 ELISA Kits)-positive breast cancer metastasis.
The protein encoded by this gene is a GTPase which belongs to the RAS superfamily of small GTP-binding proteins. Members of this superfamily appear to regulate a diverse array of cellular events, including the control of cell growth, cytoskeletal reorganization, and the activation of protein kinases.
, ras-related C3 botulinum toxin substrate 3
, rho family, small GTP binding protein Rac3
, ras-related C3 botulinum toxin substrate 3 (rho family, small GTP binding protein Rac3)