Ras-related dexamethasone-induced 1 (RASD1) is a member of the family of Ras monomeric G-proteins and was initially known as a dexamethasone inducible gene. RASD1 consists of four highly conserved guanosine-5′-triphosphate (GTP) binding and hydrolysis pockets (Σ1-Σ4) and also an effector loop. The Σ1 and Σ2 pockets comprise phosphate-magnesium binding domains and the Σ3 and Σ4 consists of guanine nucleotide binding loops. The C-terminal region of RASD1 has a cationic CAAX-domain. It is expressed in the heart, white adipose tissues, liver and kidneys.
Specificity
Anti-RASD1(C-terminal) specifically recognizes human RASD1.
Immunogen
synthetic peptide corresponding to a sequence near the C-terminus of rat RASD1, conjugated to KLH. The corresponding sequence is highly conserved in human RASD1 (83% sequence identity) and in rat RASD1 (94% sequence identity).
Application
Anti-RASD1 (C-terminal) antibody produced in rabbit may be used in immunoblotting.
Biochem/physiol Actions
Ras-related dexamethasone-induced 1 (RASD1) /Dexras1 regulates several signaling pathways such as N-methyl-d-aspartic acid receptors (NMDAR)-nitric oxide, G-protein coupled receptors (GPCRs), mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) and protein kinase C (PKC). Dexras1 is S-nitrosylated and activated by nitric oxide (NO) donors and by NMDA receptor-stimulated NO-synthesis in cortical neurons. It acts as a novel physiological target of neuronal NO synthase (nNOS). The formation of a ternary complex between nNOS, the nNOS adaptor protein CAPON and DexRAS1 has been shown to enhance the ability of nNOS to activate Dexras1. Knock-out of nNOS in mice results in a selective decrease of Dexras1 activation. NMDA receptor-stimulated NO-signaling has been shown to mediate neuronal iron homeostasis via Dexras1. An iron-uptake signaling cascade including NMDA-NO-Dexras1-peripheral benzodiazepine receptor associated protein (PAP7)-divalent metal transporter 1 (DMT1) is thought to mediate NMDA neurotoxicity. Dexras1 interacts with FE65 and can direct modulate FE65-amyloid precursor protein (APP)-mediated transcription.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Storage and Stability
For continuous use, store at 2-8 °Cfor up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers,is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation beforeuse. Working dilutions should be discarded if not used within 12 hours.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Rasd1, a small G protein with a big role in the hypothalamic response to neuronal activation
Greenwood MP, et al.
Molecular Brain, 9(1), 1-17 (2016)
NMDA receptor-nitric oxide transmission mediates neuronal iron homeostasis via the GTPase Dexras1
Cheah JH, et al.
Neuron, 51(4), 431-440 (2006)
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