AGE-4 Methylglyoxal modifiiedCatalogue number: AGE4-010
AGE-4 (Methylglyoxal-modified protein) has synergistic effects to TNF and TNF-induced apoptosis in different cell lines. Long-term incubation of proteins with glucose leads, through Schiff's base and Amadori rearrangement products, to the formation of advanced glycation end products (AGE) which are characterized by fluorescence, brown color and inter- and intra-molecular cross-linking. Recent immunological studies using anti-AGE antibodies demonstrated the presence of AGE in (i) human lens, (ii) renal proximal tubules in patients with diabetic nephropathy and chronic renal failure, (iii) atherosclerotic lesions of arterial walls, (iv) ß2-microglobulin of carpal tunnel amyloid fibril deposits in patients with hemodialysis-related amyloidosis and (v) brain tissues of patients with Alzheimer’s disease. These results suggested the potential role of AGE in normal aging and age-enhanced disease processes. AGE-4 (Methylglyoxal-modified proteins); in Western Blot no cross-reaction with glucose-modified AGEs (AGE-1), AGE-2 (Glycerolaldehyde-modified), AGE-3 (Glycolaldehyde-modified), AGE-5 (Glyoxal-modified), AGE-6 (3-DG-modified), CEL-BSA, CML-BSA and BSA.
Immunogen: Methylglyoxal-modified BSA
Protein G affinity purified monoclonal antibody in PBS with 2% Block Ace as stabilizer and 0.1% Proclin as preservative
Purification Method: Protein G affinity purified monoclonal antibody in PBS with 2% Block Ace as stabilizer and 0.1% Proclin as preservative
Concentration: 0.25 mg/ml
Secondary Reagents: As secondary system in ELISA and Western Blot we recommend biotinylated anti-mouse IgG antibody (Art. No. ZU102) in combination with streptavidin-HRPO conjugate (Art. No. ZU054) or streptavidin-alkaline phosphatase (Art. No. ZU051).
Species Reactivity: Human
Incubation Time: 60 min at RT or 18 hr at 2-8°C
Working Concentration: (liquid conc.) 0,1 µg/ml (WB) and 0,05 µg/ml (ELISA)
Positive Control: human lens, arteriosclerotic plaques
These antibodies are intended for in vitro research use only. They must not be used for clinical diagnostics and not for in vivo experiments in humans or animals.
1. Takeuchi M. , Makita Z., Bucala R., Suzuki T., Koike T., and Kameda Y. (2000) Immunological evidence that non-carboxymethyllysine Advanced Glycation End-products are produced from short chain sugars and dicarbonyl compounds in vivo. Mol. Med. 6; 114-125. 2. Takeuchi M., Yanase Y., Matsuura N., Yamagishi S., Kameda Y., Bucala R., and Z. Matika (2001) Immunological detection of a novel Advanced Glycation End-Product. Mol. Med. 7; 783-791. 3. Van Herreweghe F. et al. (2002) 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.;99(2):949-954. 4. Speer O. et al.(2003) Rapid suppression of mitochondrial permeability transition by methylglyoxal. Role of reversible arginine modification. J. Biol .Chem. 278(37):34757-63.
AGE-4 Methylglyoxal modifiied