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AGEs Rabbit pAb (bs-1158R)  
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50ul/1180.00元
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產(chǎn)品編號 bs-1158R
英文名稱 AGEs Rabbit pAb
中文名稱 晚期糖基化終末產(chǎn)物抗體
別    名 advanced glycosylation end products; AGE.  
Specific References  (17)     |     bs-1158R has been referenced in 17 publications.
[IF=14.593] Wanyi Zhou. et al. Glucose and MMP-9 dual-responsive hydrogel with temperature sensitive self-adaptive shape and controlled drug release accelerates diabetic wound healing. Bioact Mater. 2022 Jan;:  IF ;  Rat.  
[IF=7.169] Zou Ting-feng. et al. Fisetin treatment alleviates kidney injury in mice with diabetes-exacerbated atherosclerosis through inhibiting CD36/fibrosis pathway. ACTA PHARMACOL SIN. 2023 May;:1-10  IF,WB ;  Mouse.  
[IF=7.129] Juanjuan Duan. et al. Benzo[a]pyrene and a high-fat diet induce aortic injury and promote low-density lipoprotein accumulation in the endothelium. ECOTOX ENVIRON SAFE. 2023 Jul;259:115011  IHC ;  Mouse.  
[IF=6.78] Zhuozhou Hu. et al. Acyclovir alleviates insulin resistance via activating PKM1 in diabetic mice. LIFE SCI. 2022 Sep;304:120725  WB ;  Mouse.  
[IF=6.312] Hee-Weon Lee. et al. Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE. Antioxidants-Basel. 2021 Sep;10(9):1486  WB ;  Mouse.  
[IF=6.208] Haiyan Zhou. et al. Glycation of Tie-2 Inhibits Angiopoietin-1 Signaling Activation and Angiopoietin-1-Induced Angiogenesis. INT J MOL SCI. 2022 Jan;23(13):7137  IHC ;  Human.  
[IF=6.147] Dedert Cass. et al. Progranulin Preserves Autophagy Flux and Mitochondrial Function in Rat Cortical Neurons Under High Glucose Stress. FRONT CELL NEUROSCI. 2022 Jul;0:354  WB ;  Rat.  
[IF=5.27] Huang, Kaipeng, et al. "Sirt1 resists AGEs-induced expressions of FN and TGF-β1 by activating the Nrf2/ARE pathway in GMCs."?Free Radical Biology and Medicine?(2013).  WB ;  Rat.  
[IF=5.151] Kim DY et al. Eucalyptol Inhibits Advanced Glycation End Products‐Induced Disruption of Podocyte Slit Junctions by Suppressing Rage‐Erk‐C‐Myc Signaling Pathway.Mol Nutr Food Res. 2018 Oct;62(19):e1800302.  WB&IHC-P ;  Mouse.  
[IF=4.082] Eun-Jung Leeet al. Coumarin Ameliorates Impaired Bone Turnover by Inhibiting the Formation of Advanced Glycation End Products in Diabetic Osteoblasts and Osteoclasts. Biomolecules . 2020 Jul 15;10(7):1052.  WB ;  mouse.  
[IF=3.75] Andressa S. Sousa. et al. Evaluation of coronary function in female rats with severe type 1 diabetes: Effects of combined treatment with insulin and pyridoxamine. MICROVASC RES. 2022 Dec;:104474  WB ;  Rat.  
[IF=3.571] Oh H et al. Asaronic Acid Attenuates Macrophage Activation toward M1 Phenotype through Inhibition of NF-κB Pathway and JAK-STAT Signaling in Glucose-Loaded Murine Macrophages. J Agric Food Chem. 2019 Aug 26.  WB ;  Mouse.  
[IF=3.352] Wei-Yu Yeh. et al. Functional chicken-liver hydrolysates ameliorate insulin resistance and cognitive decline in streptozotocin-induced diabetic mice. Poultry Sci. 2022 Mar;:101887  WB ;  Mouse.  
[IF=3.21] Tanaka M et al. Effects of combined treatment with blood flow restriction and low intensity electrical stimulation on diabetes mellitus-associated muscle atrophy in rats.J Diabetes. (2018) Sep 18  WB ;  Calf.  
[IF=2.66] Ye, Ruidong, et al. "Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats." Neurochemistry international 58.3 (2011): 391-398.  WB ;  Rat.  
[IF=1.39] Ryuma Haraguchi et al. New Insights into the Pathogenesis of Diabetic Nephropathy: Proximal Renal Tubules Are Primary Target of Oxidative Stress in Diabetic Kidney. Acta Histochem Cytochem . 2020 Apr 28;53(2):21-31.  IHC ;  mouse.  
[IF=1.11] Lu, Lin, et al. "Effects of atorvastatin on progression of diabetic nephropathy and local RAGE and soluble RAGE expressions in rats." Journal of Zhejiang University SCIENCE B 12.8 (2011): 652-659.  WB ;  Rat.  
研究領(lǐng)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(yīng) Human,Mouse,Rat
產(chǎn)品應(yīng)用 WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/Test
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 62 kDa
檢測分子量
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
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
產(chǎn)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.

AGEs又稱非酶糖基化終末產(chǎn)物(AGEs) 是蛋白質(zhì)、脂質(zhì)和核酸等大分子的游離氨基與還原性單糖的醛基反應(yīng)所生成的穩(wěn)定的共價化合物, 在體內(nèi)的積累、增多是導致糖尿病等多種疾病及其并發(fā)癥的關(guān)鍵因素。AGEs的異常增多,可直接或間接地對機體產(chǎn)生致病作用。
晚期糖基化終末產(chǎn)物-AGEs的相關(guān)學說
晚期糖基化終末產(chǎn)物(Advanced glycation endproducts,AGEs)是一類經(jīng)由糖,包括通過Maillard反應(yīng)形成的代謝中間產(chǎn)物化學修飾的蛋白。AGEs具有高度交聯(lián)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(chǎn)物(AGEs)可引起體內(nèi)組織一系列病理生理改變,是導致糖尿病慢性并發(fā)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(xù)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(xiàn)骨質(zhì)疏松及脫鈣。
AGEs具有廣泛的致病作用。AGEs形成后引起蛋白質(zhì)分子間廣泛交聯(lián),致使蛋白質(zhì)結(jié)構(gòu)、機械強度、溶解性和配位結(jié)合等性質(zhì)均發(fā)生改變。體內(nèi)多種蛋白質(zhì)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(zhì)積聚等。AGEs與其細胞表面受體(RAGE)結(jié)合,通過趨化和活化單核巨噬細胞,激活轉(zhuǎn)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(chǎn)生氧自由基等途徑,參與糖尿病慢性并發(fā)癥的發(fā)生和發(fā)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(xù)在組織中累積。從組織AGEs自然解釋出的反應(yīng)中間物,如不能經(jīng)腎臟消除,可再次結(jié)合到其他結(jié)構(gòu)上,發(fā)生AGEs的“第二次”或“第三次”生成,致病作用加重。
產(chǎn)品圖片
25 ug total protein per lane of various lysates (see on figure) probed with AGEs polyclonal antibody, unconjugated (bs-1158R) at 1:1000 dilution and 4°C overnight incubation. Followed by conjugated secondary antibody incubation at r.t. for 60 min.
25 ug total protein per lane of various lysates (see on figure) probed with AGEs polyclonal antibody, unconjugated (bs-1158R) at 1:1000 dilution and 4°C overnight incubation. Followed by conjugated secondary antibody incubation at r.t. for 60 min.
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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