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Merck
CN

SAB4200487

Sigma-Aldrich

Anti-RASD1

enhanced validation

~1.0 mg/mL, affinity isolated antibody

别名:

Anti-AGS1, Anti-DEXRAS1, Anti-Dexamethasone-induced Ras-related protein 1

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关于此项目

UNSPSC代码:
12352203
NACRES:
NA.41
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偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

分子量

antigen ~32 kDa

种属反应性

human

增强验证

recombinant expression
Learn more about Antibody Enhanced Validation

浓度

~1.0 mg/mL

技术

western blot: 1-2 μg/mL using cell lysates of HEK-293T overexpressing human RASD1

UniProt登记号

运输

dry ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... RASD1(51655)
mouse ... Rasd1(19416)
rat ... Rasd1(64455)

一般描述

Ras-related dexamethasone-induced 1 (RASD1) belongs to the Ras family of monomeric G-proteins and was initially recognized as a dexamethasone inducible gene. RASD1 comprises an effector loop, four highly conserved guanosine-5′-triphosphate (GTP) binding and hydrolysis pockets (Σ1-Σ4). The Σ1 and Σ2 pockets have phosphate-magnesium binding domains and the Σ3 and Σ4 comprises guanine nucleotide binding loops. The C-terminal region of RASD1 includes a cationic CAAX-domain. RASD1 is expressed in the liver, heart, white adipose tissues and kidneys. The RASD1 gene is present at the human chromosome location 17p11.2.

免疫原

synthetic peptide corresponding to an internal region of human RASD1, conjugated to KLH. The corresponding sequence is identical in mouse and rat RASD1.

应用

Anti-RASD1 is suitable for use in immunoblotting.

生化/生理作用

Anti-RASD1 specifically recognizes human RASD1.
Ras-related dexamethasone-induced 1 (RASD1) /Dexras1 modulates various signaling pathways like, 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 functions as a novel physiological target of neuronal NO synthase (nNOS). The development of a ternary complex between nNOS, the nNOS adaptor protein CAPON and DexRAS1 promotes the ability of nNOS to activate Dexras1. It is S-nitrosylated, which is activated by nitric oxide (NO) donors and by NMDA receptor-stimulated NO-synthesis in cortical neurons. Knock-out of nNOS in mice results in the selective reduction of Dexras1 activation. NMDA receptor-enhanced NO-signaling mediates neuronal iron homeostasis through Dexras1. An iron-uptake signaling cascade including NMDA-NO-Dexras1-peripheral benzodiazepine receptor associated protein (PAP7)-divalent metal transporter 1 (DMT1) facilitates NMDA neurotoxicity. Dexras1 interacts with FE65 and directly regulates FE65-amyloid precursor protein (APP)-mediated transcription.

外形

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

制备说明

For continuous use, store at 2-8 °C for 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 before use. Working dilutions should be discarded if not used within 12 hours.

免责声明

Unless otherwise stated in our catalog, 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.

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储存分类代码

10 - Combustible liquids

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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分析证书(COA)

Lot/Batch Number

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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)
RASD1
Bouchard-Cannon P and Cheng HYM
Encyclopedia of Signaling Molecules, 1-9 (2017)
NMDA receptor-nitric oxide transmission mediates neuronal iron homeostasis via the GTPase Dexras1
Cheah JH, et al.
Neuron, 51(4), 431-440 (2006)
Weimin Bi et al.
Genome research, 12(5), 713-728 (2002-05-09)
Smith-Magenis syndrome (SMS) is a multiple congenital anomaly/mental retardation syndrome associated with behavioral abnormalities and sleep disturbance. Most patients have the same approximately 4 Mb interstitial genomic deletion within chromosome 17p11.2. To investigate the molecular bases of the SMS phenotype

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