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- 详细信息
- 文献和实验
- 技术资料
- 供应商:
上海联迈生物工程有限公司
- 库存:
大量
- 靶点:
详见说明书
- 级别:
1
- 目录编号:
LM-0177R-FITC
- 克隆性:
多克隆
- 抗原来源:
Rabbit
- 保质期:
1年
- 抗体英文名:
Anti-RAGE/FITC
- 抗体名:
Anti-RAGE/FITC
- 标记物:
FITC标记
- 宿主:
Human, Mouse, Rat,
- 适应物种:
Human, Mouse, Rat,
- 免疫原:
详见说明书
- 亚型:
IGg
- 形态:
粉末、液体、冻干粉
- 应用范围:
Flow-Cyt=1:50-200 ICC=1:50-200 IF=1:50-200
- 浓度:
1mg/ml
- 保存条件:
-20 °C
- 规格:
100ul
| 英文名称 | Anti-RAGE/FITC |
| 中文名称 | FITC标记的晚期糖基化终末产物特异性受体抗体 |
| 别 名 | Advanced glycosylation end product specific receptor; Advanced glycosylation end product-specific receptor; AGER; EC 2.7.11.22; LE 9211 A antigen;LE-9211-A antigen; MGC22357; MOK; RAGE 1; RAGE1; MOK protein kinase; Receptor for advanced glycation endproducts;Renal tumor antigen 1; Renal tumor antigen; Renal cell carcinoma antigen (MOK protein kinase); Renal tumor antigen 1; RAGE_HUMAN. |
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Journal PMID IF Application Mediators of Inflammation (2014) Others 3.8820 FCM Acta Pharmacologica Sinica (2014) 25152026 2.4960 FCM |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 肿瘤 心血管 免疫学 生长因子和激素 糖尿病 内分泌病 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, |
| 产品应用 | Flow-Cyt=1:50-200 ICC=1:50-200 IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 42kDa |
| 细胞定位 | 细胞膜 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from rat AGER |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 产品介绍 | background: Advanced glycosylation end product-specific receptor (AGER; RAGE) is a member of the immunoglobulin superfamily of cell surface molecules that binds molecules that have been irreversibly modified by non-enzymatic glycation and oxidation, and are know as advanced glycation end products (AGEs). It is expressed by endothelium, mononuclear phagocytes, neurons and smooth muscle cells. Whereas RAGE is present at high levels during development, especially in the central nervous system, its levels decline during maturity.The increased expression of RAGE is associated with several pathological states, such as diabetic vasculopathy, neuropathy, retinopathy and other disorders, including Alzheimer's disease and immune/inflammatory reactions of the vessel walls. In diabetic tissues, the production of RAGE is due to the overproduction of AGEs that eventually overwhelm the protective properties of RAGE. This results in oxidative stress and endothelial cell dysfunction that leads to vascular disease in diabetics. In the brain, RAGE also binds amyloid beta (Ab). Because Ab is overproduced in neurons and vessels in the brains of Alzheimer disease, this leads to the hyperstimulation of RAGE. The RAGE-Ab interaction is thought to result in oxidative stress leading to neuronal degeneration. Function: Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling. Subunit: Interacts with S100B, S100A1 and APP. Interacts with S100A12. Subcellular Location: Isoform 1: Cell membrane; Single-pass type I membrane protein. Isoform 2: Secreted. Tissue Specificity: Endothelial cells and cardiomyocytes. Similarity: Contains 2 Ig-like C2-type (immunoglobulin-like) domains. Contains 1 Ig-like V-type (immunoglobulin-like) domain. Database links: Entrez Gene: 177 Human Entrez Gene: 11596 Mouse Entrez Gene: 81722 Rat Omim: 600214 Human SwissProt: Q15109 Human SwissProt: Q62151 Mouse SwissProt: Q63495 Rat Unigene: 534342 Human Unigene: 3383 Mouse Unigene: 9829 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 晚期糖基化终末产物受体(AGER)与其配体AGEs形成的AGEs-AGER 系统在糖尿病血管病变的发生、发展过程中起着重要作用. 年龄及晚期糖基化终末产物(AGEs)等多种因素均能调节AGER基因的表达. 糖尿病患者体内晚期糖基化终末产物受体(AGER)的高表达加速了病人血管病变的发展过程,并增加了病变的复杂性.阻断AGER通路可缓解糖尿病血管的病变过程。 因此,AGER可以作为治疗糖尿病血管病变的药物靶点,并为临床治疗糖尿病血管病变提供了新的思路. |
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