| 產(chǎn)品編號(hào) | bs-0177R-AP |
| 英文名稱(chēng) | Rabbit Anti-RAGE/AP Conjugated antibody |
| 中文名稱(chēng) | 堿性磷酸酶（AP）標(biāo)記的晚期糖基化終末產(chǎn)物特異性受體抗體 |
| 別 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. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買(mǎi) 大包裝/詢(xún)價(jià) |
| 說(shuō) 明 書(shū) | 100ul |
| 研究領(lǐng)域 | 腫瘤 心血管 免疫學(xué) 生長(zhǎng)因子和激素 糖尿病 內(nèi)分泌病 |
| 抗體來(lái)源 | Rabbit |
| 克隆類(lèi)型 | Polyclonal |
| 交叉反應(yīng) | Mouse, Rat, (predicted: Human, ) |
| 產(chǎn)品應(yīng)用 | WB=1:50-200 IHC-P=1:50-200 IHC-F=1:50-200 ICC=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 42kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from rat AGER |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | 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. |
| 產(chǎn)品介紹 |
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 Omim: 600214 Human SwissProt: Q15109 Human SwissProt: Q62151 Mouse 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. 晚期糖基化終末產(chǎn)物受體(AGER)與其配體AGEs形成的AGEs-AGER 系統(tǒng)在糖尿病血管病變的發(fā)生、發(fā)展過(guò)程中起著重要作用. 年齡及晚期糖基化終末產(chǎn)物（AGEs）等多種因素均能調(diào)節(jié)AGER基因的表達(dá). 糖尿病患者體內(nèi)晚期糖基化終末產(chǎn)物受體（AGER）的高表達(dá)加速了病人血管病變的發(fā)展過(guò)程,并增加了病變的復(fù)雜性.阻斷AGER通路可緩解糖尿病血管的病變過(guò)程。 因此,AGER可以作為治療糖尿病血管病變的藥物靶點(diǎn),并為臨床治療糖尿病血管病變提供了新的思路. |
