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AGER Antibody Blocking Peptide

(bs-0177P)-500ug
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  • ¥880
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  • bs-0177P
  • 2025年10月16日
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      500ug

    产品编号bs-0177P
    英文名称AGER Antibody Blocking Peptide
    中文名称晚期糖基化终末产物特异性受体封闭多肽
    英文别名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.
    性状Lyophilized
    纯化方法HPLC
    研究领域

    Cardiovascular > Atherosclerosis > Diabetes associated

    Cardiovascular > Atherosclerosis > Vascular Inflammation > Inflammatory mediators

    Neuroscience > Neurology process > Neurodegenerative disease > Alzheimer's disease

    Neuroscience > Neurology process > Neurodegenerative disease > Alzheimer's disease > Amyloid

    Neuroscience > Sensory System > Visual system

    亚基Interacts with S100B, S100A1 and APP. Interacts with S100A12.
    亚细胞定位Isoform 1: Cell membrane; Single-pass type I membrane protein.
    Isoform 2: Secreted.
    组织特异性Endothelial cells and cardiomyocytes.
    相似性Contains 2 Ig-like C2-type (immunoglobulin-like) domains.
    Contains 1 Ig-like V-type (immunoglobulin-like) domain.
    功能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.
    保存条件Shipped at 4℃. Stored at -20℃ for one year. Avoid repeated freeze/thaw cycles.
    背景资料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.

     

     

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