晚期糖基化终末产物特异性受体抗体，Anti-AGER

英文名称  Anti-AGER 

中文名称  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. 

浓    度  1mg/1ml 

规 格  0.1ml/100μg  0.2ml/200μg  

抗体来源  Rabbit  

克隆类型  polyclonal 

晚期糖基化终末产物特异性受体抗体交叉反应  Human, Mouse, Rat, Dog, Pig, Cow 
产品类型  一抗    

研究领域  肿瘤 心血管 细胞生物 神经生物学 生长因子和激素 糖尿病 内分泌病  

蛋白分子量  predicted molecular weight: 42kDa 

性    状  Lyophilized or Liquid 

免 疫 原  KLH conjugated synthetic peptide derived from human AGER 

亚    型  IgG 

纯化方法  affinity purified by Protein A 

储 存 液  Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4 

产品应用   WB=1:100-500  ELISA=1:500-1000  IHC-P=1:100-500  IHC-F=1:100-500  Flow-Cyt=1:100-500  ICC=1:100-500  IF=1:100-500 

（石蜡切片需做抗原修复） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

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. 

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特异性受体抗体产品介绍 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. 

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.