RAS, Dexamethasone-Induced 1 (RASD1) Kits ELISA

Human RAS, Dexamethasone-Induced 1 (RASD1) interaction partners

1. Via a feedback loop involving miR-375, RASD1, and ERalpha.

2. These findings suggest that the upregulation of RASD1 in glioma tissues may play an inhibitory role in tumor expansion, possibly through inactivating the AKT/mTOR signaling pathway.

3. Studies indicate potential roles for Rasd1 small G protein and leptin in TRPC4 cation channel activation.

4. Data indicate that protein kinase A (PKA) phosphorylates only serine-253 amino acid on activator of G-protein signaling 1 protein Dexras1 (RASD1).

5. Loss of RASD1 is associated with prostate cancer.

6. Study showed that Rasd1 and NonO interact at the CRE-site of specific target genes.

7. Rasd1 modulates endogenous renin gene expression by interacting with Ear2.

8. A glucocorticoid response element (GRE) was identified in the 3'-flanking region (2.3 kb downstream of poly(A) signal) of the human Dexras1 gene. A point mutation within the 15-bp GRE abolished this glucocorticoid responsiveness

9. plays an active role in preventing aberrant cell growth

10. yeast two hybrid analysis and co-immunoprecipitation studies in mammalian cells demonstrate a direct interaction between AGS1 and the G(beta1) subunit of heterotrimeric G proteins

11. does not alter the membrane translocation of protein kinase C delta.

12. Dexras1 plays a critical role in shaping the photic phase response curve (PRC) and the signaling events through which it regulates clock entrainment in transgenic mice.

13. dex-ras1 mRNA is not induced by glucocorticoid stimulation in HEK293 cells

14. Dexras1 functions as a suppressor of FE65-APP-mediated transcription, and FE65 tyrosine 547 phosphorylation enhances FE65-APP-mediated transcription, at least in part, by modulating the interaction between FE65 and Dexras1

15. Epigenetic inactivation of genes, including RASD1, plays a key role in the development of dexamethasone resistance in multiple myeloma.

Mouse (Murine) RAS, Dexamethasone-Induced 1 (RASD1) interaction partners

1. These results suggest that Dexras1 is a critical mediator of the IGF-1 signal to activate MAPK, linking glucocorticoid signaling to IGF-1 signaling in adipogenesis.

2. These findings suggest that RASD1 acts as a novel signaling molecule and plays an important role in regulating dynamic uterine remodeling during the estrous cycle in the uterus.

3. This study demonstrated that provide unprecedented evidence for a selective epigenetic up-regulation of Dexras 1 gene expression in the striatum of EAE mice.

4. RASD1 is a novel factor in Metaphase I-Metaphase II oocyte transition and may be involved in regulating the progression of cytokinesis and spindle formation

5. Results suggest a potential role for Dexras1 in modulating a selective subset of psychiatric symptoms, possibly via its interaction with NMDARs and/or other disease-related binding-partners

6. two mechanisms of Rasd1 induction in the hypothalamus, were identified.

7. Lysosomal iron modulates NMDA receptor-mediated excitation via small GTPase, Dexras1

8. Dexras1 mediates adipogenesis and diet-induced obesity.

9. Dexras1 is involved in the circadian clock regulation

10. Dexras1 appears to mediate N-methylaspartate (NMDA)-elicited neurotoxicity via nitric oxide and iron influx.

11. These results indicate that the absence of Dexras1 sensitizes the suprachiasmatic nucleus to perturbations resulting from restricted feeding.

12. Data suggest that Dexras1 regulates multiple photic and nonphotic signal-transduction pathways, thereby playing an essential role modulating species-specific characteristics of circadian entrainment.

13. Rasd1 modulates endogenous renin gene expression by interacting with Ear2.

14. the Dexamethasone-induced RAS protein 1 (Dexras1) gene is a cycling gene in the suprachiasmatic nucleus

15. Genetic deletion of Dexras1 reduces photic entrainment by eliminating a pertussis-sensitive circadian response to NMDA. Mechanistically, Dexras1 couples NMDA and light input to Gi/o and ERK activation. In

16. dexras1 was found to change rhythmically in hypothalamic and extra-hypothalamic brain regions reaching peak levels early in the light phase.

17. We demonstrate that Rasd1 mRNA is expressed in mouse lymph node cells in response to inhibitory stimuli. Rasd1 mRNA is present at low levels in freshly isol. cells, but it is up-regulated in culture and is expressed in cells whose proliferation is blocked