Increasing evidence points to the adverse effects of advanced glycation end product modified proteins on aging-related human health. AGE modified proteins result from the non-enzymatic glycosylation of glucose with free protein amino groups reaction of carbohydrates via Maillard reaction, including advanced product formation following Amadori rearrangements. AGE accumulation is thought to contribute to pathological changes resulting in cataract formation, Alzheimer‘s disease, osteoarthritis, and myocardial dysfunction. Diabetes (hyperglycemia) is associated with accelerated of AGE formation.
Human aorta atherosclerotic lesion:
(Usage concentration 3µg/mL)
Anti-CML monoclonal antibody(NF-1G) has a ten times better sensibility than a former
Anti-CML monoclonal antibody(CMS-10).
This antibody is a monoclonal that very specific to CML and don’t recognize CEL and very useful for localyzed analysis in immunohistochemistry.
Renal proximal tubule and glomerulus in
patients with diabetic nephropathy.
Result of an anti AGE antibody analysis, shows that AGE accumulates the following parts of (1) human lens (nondiabetic and noncataractous), (2) renal proximal tubules in patients with diabetic nephropathy and chronic renal failure,(3) diabetic retina, (4) peripheral nerves of diabetic neuropathy, (5) atherosclerotic lesions of arterial walls, (6)ﾟ2-microglobulin forming amyloid fibrils in patients with hemodialysis-related amyloidosis, (7) senile plaques of patients with Alzheimer痴 disease, (8) the peritoneum of CAPD patients, (9) skin elastin in actinic elastosis, and (10) ceriod/lipofuscin deposits. These evidence suggests that AGE is deeply involved with Aging itself and chronic disease caused by an aging, and several AGE structure give emphasis to diabetes and brain disease field category. Various antibody Currently Proposed as AGE is CML,CEL, Pentosidine, Pyrraline, Imidazolone, Crossline and others.
To be used for research only. DO NOT use for human gene therapy or clinical diagnosis!