| 中文名稱 | 晚期糖基化終末產物抗體 |
| 別 名 | advanced glycosylation end products; AGE. |
| 研究領域 | 細胞生物 免疫學 糖尿病 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應 | Human, Rat, (predicted: Mouse, ) |
| 產品應用 | ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1ug/Test IF=1:100-500 （石蠟切片需做抗原修復） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 細胞定位 | 分泌型蛋白 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | AGEs: |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. |
| PubMed | PubMed |
| 產品介紹 | Advanced Glycation End products (AGEs) are the result of a chain of chemical reactions after an initial glycation reaction. The intermediate products are known, variously, as Amadori, Schiff base and Maillard products, named after the researchers who first described them. (The literature is inconsistent in applying these terms. For example, Maillard reaction products are sometimes considered intermediates and sometimes end products.) Side products generated in intermediate steps may be oxidizing agents (such as hydrogen peroxide), or not (such as beta amyloid proteins).[1] "Glycosylation" is sometimes used for "glycation" in the literature, usually as 'non-enzymatic glycosylation. The AGE modified BSA was produced by reacting BSA with glycolaldehyde under sterile conditions followed by extensive dialysis and purification steps. SWISS: P02769 Gene ID: AGEs Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. AGEs又稱非酶糖基化終末產物(AGEs) 是蛋白質、脂質和核酸等大分子的游離氨基與還原性單糖的醛基反應所生成的穩定的共價化合物, 在體內的積累、增多是導致糖尿病等多種疾病及其并發癥的關鍵因素。AGEs的異常增多，可直接或間接地對機體產生致病作用。 晚期糖基化終末產物-AGEs的相關學說 晚期糖基化終末產物（Advanced glycation endproducts，AGEs）是一類經由糖，包括通過Maillard反應形成的代謝中間產物化學修飾的蛋白。AGEs具有高度交聯性。 AGE與AGE受體（如RAGE）的相互作用誘導了受體承載細胞核因子-κB（NF—κB）的活化，同時這一作用還誘導了細胞因子、生長因子及黏附分子表達的增加。 在糖尿病方面，晚期糖基化終末產物(AGEs)可引起體內組織一系列病理生理改變,是導致糖尿病慢性并發癥的重要致病因素。在健康人群中AGEs也隨年齡增加在組織中持續積累,并參與衰老過程。由于糖尿病和衰老均可導致骨代謝紊亂,甚至出現骨質疏松及脫鈣。 AGEs具有廣泛的致病作用。AGEs形成后引起蛋白質分子間廣泛交聯，致使蛋白質結構、機械強度、溶解性和配位結合等性質均發生改變。體內多種蛋白質糖基化可從多個方面影響機體，如引起血管通透性增大、血管基底膜增厚和細胞外基質積聚等。AGEs與其細胞表面受體（RAGE）結合，通過趨化和活化單核巨噬細胞，激活轉錄因子NF-KB，促進細胞因子和組織因子的釋放，滅活一氧化氮和產生氧自由基等途徑，參與糖尿病慢性并發癥的發生和發展 。由于AGEs的不可逆性，即使高血糖被糾正后，AGEs水平也不能回復到正常，而繼續在組織中累積。從組織AGEs自然解釋出的反應中間物，如不能經腎臟消除，可再次結合到其他結構上，發生AGEs的“第二次”或“第三次”生成，致病作用加重。 |
| 產品圖片 |  Tissue/cell: Rat kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded;Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(bs-1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining  Tissue/cell: rat kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded;Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(bs-1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining  Blank control: MCF7.Primary Antibody (green line): Rabbit Anti-AGEs antibody (bs-1158R) Dilution: 1μg /10^6 cells; Isotype Control Antibody (orange line): Rabbit IgG . Secondary Antibody : Goat anti-rabbit IgG-AF647 Dilution: 1μg /test. Protocol The cells were incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed. |
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