RAGE重组兔单抗

bsm-52809R

重组兔单抗、mIHC精品抗体

RAGE Recombinant Rabbit mAb

RAGE重组兔单抗

RAGE; SCARJ1; sRAGE; RAGE_HUMAN; AGER; Receptor for advanced glycosylation end products; RAGE_MOUSE; RAGE_RAT;

Rabbit

KLH conjugated synthetic peptide derived from mouse RAGE

IgG

Liquid

affinity purified by Protein A

Recombinant

8G4

42 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

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.

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.