useful for research of diabetes, chromic diseases associated with aging and diabetic complications, cell death

Anti AGE-4 Monoclonal Antibody


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Background

The products of the nonenzymatic glycation and oxidation of proteins, lipids and nucleic acids, the advanced glycation end-products (AGEs), accumulate in various pathological conditions, such as diabetes, inflammation, renal failure, and aging. AGEs accumulate at site of microvascular injury in diabetes, including the kidney, the retina, and within the vasculature. The enhanced formation of AGEs also exists in various disease, such as atherosclerosis, Alzheimer’s disease, end-stage renal disease (ESRD), rheumatoid arthritis and liver cirrhosis.
AGEs can arise not only from glucose, but also from dicarbonyl compounds, short chain-reducing sugars and other metabolic pathways of glucose. Methylglyoxal (MG) increases in diabetes and can modify proteins rapidly and form AGE-4. It has been showed that exogenously added MG has a strong synergistic effect on TNF-induced cell death and AGE-4 is formed during TNF-induced cell in death mouse L929 cell, and that increased MG and AGE-4 levels induce apoptosis in mycobacterial-infected macrophages. It also has been demonstrated that MG rapidly modifies the PTP covalently and stabilizes the PTP in the closed conformation in rat liver mitochondria. Moreover, it has been showed that an increase in intracellular MG concentration inhibit the insulin signaling pathway and leads to an insulin-resistant state in L6 muscle cells.
This antibody is specific to AGE-4 and will be useful to research for diabetes, chromic diseases associated with aging and diabetic complications, cell death


 AGEs Antibody Flyer [PDF]
 AGEs Antibody Flyer@(print file) [PDF]

Application

WB 0.1 μg/mL
IHC Not tested
ICC Not tested
ELISA 0.05 μg/mL
FCM Not tested
Neutralization Not tested
IP Not tested

<References>
1. Takeuchi M. et al.: Immunological evidence that non-carboxymethyllysine advanced glycation end-products are produced from short chain sugars and dicarbonyl compounds in vivo. Mol Med. 2000 Feb;6(2):114-25.
2. Takeuchi M. et al.: Immunological detection of a novel advanced glycation end-product. Mol Med. 2001 Nov;7(11):783-91.
3. Van Herreweghe F. et al.: Tumor necrosis factor-induced modulation of glyoxalase I activities through phosphorylation by PKA results in cell death and is accompanied by the formation of a specific methylglyoxal-derived AGE. Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):949-54. Epub 2002 Jan 15.
4. Speer O. et al.: Rapid suppression of mitochondrial permeability transition by methylglyoxal. Role of reversible arginine modification. J Biol Chem. 2003 Sep 12;278(37):34757-63. Epub 2003 Jun 18.
5. Riboulet-Chavey A. et al.: Methylglyoxal impairs the insulin signaling pathways independently of the formation of intracellular reactive oxygen species. Diabetes. 2006 May;55(5):1289-99.
6. Rachman H. et al.: Critical role of methylglyoxal and AGE in mycobacteria-induced macrophage apoptosis and activation.PLoS ONE. 2006 Dec 20;1:e29.

This product is generated from GANP® mice

Product List

Product Name Cat# Quantity Price

Anti AGE-4, - (Mouse) Unlabeled DataSheet

KAL-KG133

10 UG ¥55,000
$734