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RASD1 encodes a member of the Ras superfamily of small GTPases and is induced by dexamethasone. Additionally we are shipping RASD1 Antibodies (28) and RASD1 Kits (4) and many more products for this protein.
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Studies indicate potential roles for Rasd1 small G protein (show RAC2 Proteins) and leptin (show LEP Proteins) in TRPC4 (show TRPC4 Proteins) cation channel (show TRPV1 Proteins) activation.
Data indicate that protein kinase A (PKA) phosphorylates only serine-253 amino acid on activator of G-protein signaling 1 protein Dexras1 (RASD1).
Loss of RASD1 is associated with prostate cancer.
Study showed that Rasd1 and NonO (show NONO Proteins) interact at the CRE-site of specific target genes.
Rasd1 modulates endogenous renin (show REN Proteins) gene expression by interacting with Ear2 (show NR2F6 Proteins).
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
yeast two hybrid analysis and co-immunoprecipitation studies in mammalian cells demonstrate a direct interaction between AGS1 (show TREX1 Proteins) and the G(beta1) subunit of heterotrimeric G proteins
does not alter the membrane translocation of protein kinase C delta (show PKCd Proteins).
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.
dex-ras1 mRNA is not induced by glucocorticoid stimulation in HEK293 cells
two mechanisms of Rasd1 induction in the hypothalamus, were identified.
Lysosomal iron modulates NMDA receptor-mediated excitation via small GTPase (show RACGAP1 Proteins), Dexras1
Dexras1 mediates adipogenesis and diet-induced obesity.
Dexras1 is involved in the circadian clock regulation
Dexras1 appears to mediate N-methylaspartate (NMDA)-elicited neurotoxicity via nitric oxide and iron influx.
These results indicate that the absence of Dexras1 sensitizes the suprachiasmatic nucleus to perturbations resulting from restricted feeding.
Data suggest that Dexras1 regulates multiple photic and nonphotic signal-transduction pathways, thereby playing an essential role modulating species-specific characteristics of circadian entrainment.
the Dexamethasone-induced RAS protein 1 (Dexras1) gene is a cycling gene in the suprachiasmatic nucleus
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 (show EPHB2 Proteins) activation. In
This gene encodes a member of the Ras superfamily of small GTPases and is induced by dexamethasone. The encoded protein is an activator of G-protein signaling and acts as a direct nucleotide exchange factor for Gi-Go proteins. This protein interacts with the neuronal nitric oxide adaptor protein CAPON, and a nuclear adaptor protein FE65, which interacts with the Alzheimer's disease amyloid precursor protein. This gene may play a role in dexamethasone-induced alterations in cell morphology, growth and cell-extracellular matrix interactions. Epigenetic inactivation of this gene is closely correlated with resistance to dexamethasone in multiple myeloma cells. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
activator of G-protein signaling 1
, dexamethasone-induced Ras-related protein 1
, ras-related protein
, DEXRAS1 (Dexras1)