anti-RAS Guanyl Releasing Protein 3 (Calcium and DAG-Regulated) (RASGRP3) Antibodies

Human RAS Guanyl Releasing Protein 3 (Calcium and DAG-Regulated) (RASGRP3) interaction partners

1. In conclusion, these findings provide a new insight into the upregulation of RasGRP3 involved in Notch pathway activation in the development of esophageal squamous cell carcinoma , especially under nutrient deprivation.

2. The marked differences between RasGRP3 and RasGRP1 in membrane interaction necessarily will contribute to their different behavior in cells.

3. these data show that RasGRP3 exerts its oncogenic effect in papillary thyroid cancer through Akt-mediated MDM2 activation.

4. RasGRP3 mediates ERK MAPK pathway activation in GNAQ mutant uveal melanoma.

5. Knockdown of RasGRP3 inhibited proliferation in prostate neoplasms.

6. 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.

7. The identification of the role of RasGRP3 in melanoma highlights its importance, as a Ras activator, in the phosphoinositide signaling pathway in human melanoma.

8. 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

9. RasGRP3 contributes to the malignant phenotype of prostate cancer cells and may constitute a novel therapeutic target for human prostate cancer.

10. A vascular gene trap screen defines RASGRP3 as an angiogenesis-regulated gene required for the endothelial response to phorbol esters.

11. studies support the hypothesis that RasGRP phosphorylation by PKC is a mechanism that integrates DAG signaling systems in T and B cells

12. dynein light chain 1 represents a novel anchoring protein for RasGRP3 that may regulate subcellular localization of the exchange factor

Mouse (Murine) RAS Guanyl Releasing Protein 3 (Calcium and DAG-Regulated) (RASGRP3) interaction partners

1. RasGRP1/3-deficient progenitors show impaired migration toward the CCR9 ligand, CCL25, suggesting that RasGRP1 and RasGRP3 may regulate progenitor entry into the thymus through a CCR9-dependent mechanism.

2. RasGRP3 limits inflammatory response by activating Rap1 on low-intensity pathogen infection, setting a threshold for preventing excessive inflammatory response.

3. RasGRP1, but not RasGRP3, is required for thymocyte positive selection and invariant natural killer T cell selection.

4. Expressed in developing blood vessels, Rasgrp3 contributes to the incidence of cardiovascular defects found in embryos from diabetic mothers.