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Members of the RAS (see HRAS\; MIM 190020) subfamily of GTPases function in signal transduction as GTP/GDP-regulated switches that cycle between inactive GDP- and active GTP-bound states. Additionally we are shipping RASGRP3 Antibodies (42) and RASGRP3 Proteins (6) and many more products for this protein.
these data show that RasGRP3 exerts its oncogenic effect in papillary thyroid cancer through Akt (show AKT1 ELISA Kits)-mediated MDM2 (show MDM2 ELISA Kits) activation.
RasGRP3 mediates ERK MAPK (show MAPK1 ELISA Kits) pathway activation in GNAQ (show GNAQ ELISA Kits) mutant uveal melanoma.
Knockdown of RasGRP3 inhibited proliferation in prostate neoplasms.
Ras activator RasGRP3 may have a role in the pathological behavior of breast cancer cells and may constitute a therapeutic target for human breast cancer.
The identification of the role of RasGRP3 in melanoma highlights its importance, as a Ras activator, in the phosphoinositide signaling pathway in human melanoma.
Significant associations were found for the single nucleotide polymorphism rs13385731 of RasGRP3 with malar rash, discoid rash, and antinuclear antibody in patients with systemic lupus erythematosus
RasGRP3 contributes to the malignant phenotype of prostate cancer cells and may constitute a novel therapeutic target for human prostate cancer.
A vascular gene trap screen defines RASGRP3 as an angiogenesis-regulated gene required for the endothelial response to phorbol esters.
studies support the hypothesis that RasGRP phosphorylation by PKC is a mechanism that integrates DAG signaling systems in T and B cells
dynein light chain 1 represents a novel anchoring protein for RasGRP3 that may regulate subcellular localization of the exchange factor
RasGRP1 (show RASGRP1 ELISA Kits)/3-deficient progenitors show impaired migration toward the CCR9 (show CCR9 ELISA Kits) ligand, CCL25 (show CCL25 ELISA Kits), suggesting that RasGRP1 (show RASGRP1 ELISA Kits) and RasGRP3 may regulate progenitor entry into the thymus through a CCR9 (show CCR9 ELISA Kits)-dependent mechanism.
RasGRP3 limits inflammatory response by activating Rap1 on low-intensity pathogen infection, setting a threshold for preventing excessive inflammatory response.
RasGRP1 (show RASGRP1 ELISA Kits), but not RasGRP3, is required for thymocyte positive selection and invariant natural killer T cell selection.
Expressed in developing blood vessels, Rasgrp3 contributes to the incidence of cardiovascular defects found in embryos from diabetic mothers.
Members of the RAS (see HRAS\; MIM 190020) subfamily of GTPases function in signal transduction as GTP/GDP-regulated switches that cycle between inactive GDP- and active GTP-bound states. Guanine nucleotide exchange factors (GEFs), such as RASGRP3, serve as RAS activators by promoting acquisition of GTP to maintain the active GTP-bound state and are the key link between cell surface receptors and RAS activation (Rebhun et al., 2000
RAS guanyl releasing protein 3 (calcium and DAG-regulated)
, ras guanyl-releasing protein 3
, ras guanyl-releasing protein 3-like
, calcium and DAG-regulated guanine nucleotide exchange factor III
, guanine nucleotide exchange factor for Rap1
, RAS, guanyl releasing protein 3