Application: ELISA, IHC, WB
Clonality: Monoclonal
Host: Mouse
Purification: Purified - Affinity
Reaction of protein amino groups with glucose leads, through the early products such as a Schiff base and Amadori rearrangement products, to the formation of advanced glycation end products (AGEs). Recent immunological studies using anti-AGEs antibody (6D12) demonstrated the presence of AGEs-modified proteins in several human tissues: human lens (nondiabetic and noncataractous), ( patients with diabetic nephropathy and chronic renal failure, renal proximal tubules in diabetic retina, diabetic neuropathy, atherosclerotic lesions of arterial walls, peripheral nerves of 2-microglobulin forming amyloid fibrils in patients with hemodialysis-related amyloidosis, the peritoneum of CAPD patients, senile plaques of patients with Alzheimer’s disease, ( ) skin elastin in actinic elastosis, andceriod/lipofuscin deposits. These results suggest a potential role of AGEs-modification in normal aging as well as age-enhanced disease processes. This antibody named as 6D12 has been used to demonstrate AGEs-modified proteins in these human tissues, indicating potential usefulness of this antibody for histochemical identification and biochemical quantification of AGEs-modified proteins.
Clonality: Monoclonal
Host: Mouse
Purification: Purified - Affinity
Reaction of protein amino groups with glucose leads, through the early products such as a Schiff base and Amadori rearrangement products, to the formation of advanced glycation end products (AGEs). Recent immunological studies using anti-AGEs antibody (6D12) demonstrated the presence of AGEs-modified proteins in several human tissues: human lens (nondiabetic and noncataractous), ( patients with diabetic nephropathy and chronic renal failure, renal proximal tubules in diabetic retina, diabetic neuropathy, atherosclerotic lesions of arterial walls, peripheral nerves of 2-microglobulin forming amyloid fibrils in patients with hemodialysis-related amyloidosis, the peritoneum of CAPD patients, senile plaques of patients with Alzheimer’s disease, ( ) skin elastin in actinic elastosis, andceriod/lipofuscin deposits. These results suggest a potential role of AGEs-modification in normal aging as well as age-enhanced disease processes. This antibody named as 6D12 has been used to demonstrate AGEs-modified proteins in these human tissues, indicating potential usefulness of this antibody for histochemical identification and biochemical quantification of AGEs-modified proteins.
| Documents & Links for Anti AGEs mAb (Clone 6D12) | |
| Datasheet | kal-kh001_anti-ages-mab-clone-6d12_datasheet.pdf |
| Documents & Links for Anti AGEs mAb (Clone 6D12) | |
| Datasheet | kal-kh001_anti-ages-mab-clone-6d12_datasheet.pdf |
| Citations for Anti AGEs mAb (Clone 6D12) – 7 Found |
| Kim et al. 2019. Improvement in Diabetic Retinopathy through Protection against Retinal Apoptosis in Spontaneously Diabetic Torii Rats Mediated by Ethanol Extract of Osteomeles schwerinae C.K. Schneid. Nutrients. 11(3):E546. PubMed, Journal |
| Moschonas et al. 2014. Impact of diet-induced obesity in male mouse reproductive system: The role of advanced glycation end product-receptor for advanced glycation end product axis. Exp Biol Med (Maywood). 239(8):937-47. PubMed, Journal |
| Tsakiri et al. 2013. Differential regulation of proteasome functionality in reproductive vs. somatic tissues of Drosophila during aging or oxidative stress. FASEB J. 27(6):2407-20. PubMed, Journal |
| Cabreiro et al. 2011. Increased life span from overexpression of superoxide dismutase in Caenorhabditis elegans is not caused by decreased oxidative damage. Free Radic Biol Med. 51(8):1575-82. PubMed, Journal |
| Baba et al. 2011. Aldose reductase (AKR1B3) regulates the accumulation of advanced glycosylation end products (AGEs) and the expression of AGE receptor (RAGE). Chem Biol Interact. 191(1-3):357-63. PubMed, Journal |
| Wu et al. 2011. Advanced glycation end products and its receptor (RAGE) are increased in patients with COPD. Respir Med. 105(3):329-36. PubMed, Journal |
| Baba et al. 2009. Reductive metabolism of AGE precursors: a metabolic route for preventing AGE accumulation in cardiovascular tissue. Diabetes. 58(11):2486-97. PubMed, Journal |