Rabbit Anti-AGEs antibody | Sunlong Medical

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advanced glycosylation end products; AGE.

Cat:

SL1158R

Species Reactivity：

Human,Mouse,Rat,

Immunogen：

AGEs

Format：

Liquid

Storage instructions：

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

Concentration：

1mg/ml

Clonality：

Polyclonal

Isotype：

IgG

Applications：

WB=1:500-2000ELISA=1:5000-10000IHC-P=1:100-500IHC-F=1:100-500Flow-Cyt=1ug/TestIF=1:100-500（Paraffin sections need to do antigen repair）not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.

Host：

Rabbit

Product Overview：

Sample: Lane 1: Kidney (Mouse) Tissue Lysate at 40 ugLane 2: Lung (Mouse) Tissue Lysate at 40 ugLane 3: Large intestine (Mouse) Tissue Lysate at 40 ugLane 4: Testis (Rat) Tissue Lysate at 40 ugLane 5: Lung (Rat) Tissue Lysate at 40 ugLane 6: Large intestine (Rat) Tissue Lysate at 40 ugLane 7: U87MG (Human) Cell Lysate at 30 ugPrimary: Anti-AGEs (SL1158R) at 1/1000 dilutionSecondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilutionObserved band size: 62 kDTissue/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,SLC0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(SLC0010) stainingTissue/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,SLC0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(SLC0010) stainingBlank control: MCF7. Primary Antibody (green line): Rabbit Anti-AGEs antibody (SL1158R) Dilution: 1μg /10^6 cells; Isotype Control Antibody (orange line): Rabbit IgG . Secondary Antibody : Goat anti-rabbit IgG-AF647Dilution: 1μg /test. ProtocolThe 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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Unit:

Price: $220.00

Product PDFs

Datasheet: Down Datasheet

Other Information
Citations
Protein Attributes
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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

AGEs又称非酶糖基化终末产物(AGEs) 是蛋白质、脂质和核酸等大分子的游离氨基与还原性单糖的醛基反应所生成的稳定的共价化合物, 在体内的积累、增多是导致糖尿病等多种疾病及其并发症的关键因素。AGEs的异常增多，可直接或间接地对机体产生致病作用。
晚期糖基化终末产物-AGEs的相关学说
晚期糖基化终末产物（Advanced glycation endproducts，AGEs）是一类经由糖，包括通过Maillard反应形成的代谢中间产物化学修饰的蛋白。AGEs具有高度交联性。 AGE与AGE受体（如RAGE）的相互作用诱导了受体承载细胞核因子-κB（NF—κB）的活化，同时这一作用还诱导了细胞因子、生长因子及黏附分子表达的增加。
在糖尿病方面，晚期糖基化终末产物(AGEs)可引起体内组织一系列病理生理改变,是导致糖尿病慢性并发症的重要致病因素。在健康人群中AGEs也随年龄增加在组织中持续积累,并参与衰老过程。由于糖尿病和衰老均可导致骨代谢紊乱,甚至出现骨质疏松及脱钙。
AGEs具有广泛的致病作用。AGEs形成后引起蛋白质分子间广泛交联，致使蛋白质结构、机械强度、溶解性和配位结合等性质均发生改变。体内多种蛋白质糖基化可从多个方面影响机体，如引起血管通透性增大、血管基底膜增厚和细胞外基质积聚等。AGEs与其细胞表面受体（RAGE）结合，通过趋化和活化单核巨噬细胞，激活转录因子NF-KB，促进细胞因子和组织因子的释放，灭活一氧化氮和产生氧自由基等途径，参与糖尿病慢性并发症的发生和发展。由于AGEs的不可逆性，即使高血糖被纠正后，AGEs水平也不能回复到正常，而继续在组织中累积。从组织AGEs自然解释出的反应中间物，如不能经肾脏消除，可再次结合到其他结构上，发生AGEs的“第二次”或“第三次”生成，致病作用加重。 Picture

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,SLC0005) at 37℃ for 20 min;
Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(SLC0010) 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,SLC0005) at 37℃ for 20 min;
Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(SLC0010) staining

Blank control: MCF7.
Primary Antibody (green line): Rabbit Anti-AGEs antibody (SL1158R)
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.

Product Feedback Wall

Specific References (11) | SL1158R has been referenced in 11 publications.

[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.

PubMed:10.1016/j.psj.2022.101887

[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.

PubMed:10.1016/j.bioactmat.2022.01.004

[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.

PubMed:10.3390/antiox10091486

[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.

PubMed:32679814

[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.

PubMed:32410750

[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.

PubMed:31422663

[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):e360302. WB&IHSLCP ; Mouse.

PubMed:29987888

[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.

PubMed:21791366

[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.

PubMed:30225988

[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.

PubMed:21185898

[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.

PubMed:23891678