AGER Antibody [Alexa Fluor™ Plus 555] Summary
| Specificity |
Detects canine RAGE in ELISAs and Western blots. In sandwich immunoassays, approximately 0.5% cross‑reactivity with recombinant human RAGE is observed and less than 0.1% cross-reactivity with recombinant mouse RAGE and recombinant rat RAGE is observed. |
| Isotype |
IgG |
| Clonality |
Polyclonal |
| Host |
Sheep |
| Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Packaging, Storage & Formulations
| Storage |
Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied |
| Buffer |
Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide. |
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for AGER Antibody [Alexa Fluor™ Plus 555]
Background
Advanced glycation endproducts (AGEs) are adducts formed by the non-enzymatic glycation of macromolecules. AGE formation is accelerated in oxidative and hyperglycemic conditions, diabetes, renal failure, atherosclerosis, Alzheimer’s disease, arthritis, and in normal aging (1‑5). Receptor for advanced glycation endproducts (RAGE) is a 35 kDa type I transmembrane protein belonging the immunoglobulin superfamily. Besides AGEs, RAGE binds beta -amyloid peptide, S100/calgranulin family proteins, HMGB1/amphoterin, and leukocyte integrins (6‑9). Mature canine RAGE consists of a 383 amino acid (aa) extracellular domain (ECD) with one Ig-like V-type domain and two Ig-like C‑type domains, a 23 aa transmembrane segment, and a 43 aa cytoplasmic domain (10). Within the ECD, canine RAGE shares 73%‑77% aa sequence identity with human, mouse, and rat RAGE. In human, soluble forms of RAGE are generated by alternate splicing and are associated with multiple disease states (11, 12). RAGE is expressed in the embryonic central nervous system and on macrophages, monocytes, smooth muscle cells, and endothelial cells (13‑15). It is upregulated in response to AGE accumulation, and its activation induces a broad proinflammatory response (6, 15). The increased production of reactive oxygen species during inflammation promotes additional AGE formation and RAGE upregulation, a cycle that exacerbates diabetic complications and inflammation‑induced tissue injury (2, 4).
- Schleicher, E. and U. Friess (2007) Kidney Int. Suppl. 106:S17.
- Herold, K. et al. (2007) J. Leukoc. Biol. 82:204.
- Thornalley, P.J. (2006) J. Ren. Nutr. 16:178.
- Goldin, A. et al. (2006) Circulation 114:597.
- Ramasamy, R. et al. (2005) Glycobiology 15:16R.
- Kislinger, T. et al. (1999) J. Biol. Chem. 274:31740.
- Yan, S.D. et al. (1996) Nature 382:685.
- Huttenen, H. et al. (2000) J. Biol. Chem. 275:40096.
- Chavakis, T. et al. (2003) J. Exp. Med. 198:1507.
- Murua Escobar, H. et al. (2006) Gene 369:45.
- Yonekura H, et al. (2003) Biochem. J. 370:1097.
- Koyama, H. et al. (2007) Mol. Med. 13:625.
- Hori, O. et al. (1995) J. Biol. Chem. 270:25752.
- Brett, J. et al. (1993) Am. J. Pathol. 143:1699.
- Bierhaus, A. et al. (2006) Curr. Opin. Investig. Drugs 7:985.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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