Wed. Jan 21st, 2026

Name :
RAGE Protein

Description :
Receptor for Advanced Glycosylation End Products (RAGE, or AGER) is a member of the immunoglobulin super-family transmembrane proteins, as a signal transduction receptor which binds advanced glycation endproducts, certain members of the S100/calgranulin family of proteins, high mobility group box 1 (HMGB1), advanced oxidation protein products, and amyloid (beta-sheet fibrils). Initial studies investigating the role of RAGE in renal dysfunction focused on diabetes, neurodegenerative disorders, and inflammatory responses. However, RAGE also has roles in the pathogenesis of renal disorders that are not associated with diabetes, such as obesity-related glomerulopathy, doxorubicin-induced nephropathy, hypertensive nephropathy, lupus nephritis, renal amyloidosis, and ischemic renal injuries. RAGE represents an important factor in innate immunity against pathogens, but it also interacts with endogenous ligands, resulting in chronic inflammation. RAGE signaling has been implicated in multiple human illnesses, including atherosclerosis, arthritis, Alzheimer’s disease, atherosclerosis and aging associated diseases.

Species :
Mouse

Uniprotkb :
HEK293

Tag :
His

Synonyms :
advanced glycosylation end product-specific receptor, RAGE

Construction :
A DNA sequence encoding the extracellular domain of mouse AGER (NP_031451.2) extracellular domain (Met 1-Ala 342) was expressed, with a polyhistidine tag at the C-terminus.

Protein Purity :
≥ 96 % as determined by SDS-PAGE. ≥ 85 % as determined by SEC-HPLC.

Molecular Weight :
Approxiamtely 35.3 kDa

Endotoxin :

Formulatione :
Lyophilized from sterile PBS, pH 7.4. Please contact us for any concerns or special requirements. Normally 5 % – 8 % trehalose, mannitol and 0. 01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hard copy of CoA.

Reconstitution :
A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.

Stability & Storage :
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Shipping :
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.

Research Background :
Receptor for Advanced Glycosylation End Products (RAGE, or AGER) is a member of the immunoglobulin super-family transmembrane proteins, as a signal transduction receptor which binds advanced glycation endproducts, certain members of the S100/calgranulin family of proteins, high mobility group box 1 (HMGB1), advanced oxidation protein products, and amyloid (beta-sheet fibrils). Initial studies investigating the role of RAGE in renal dysfunction focused on diabetes, neurodegenerative disorders, and inflammatory responses. However, RAGE also has roles in the pathogenesis of renal disorders that are not associated with diabetes, such as obesity-related glomerulopathy, doxorubicin-induced nephropathy, hypertensive nephropathy, lupus nephritis, renal amyloidosis, and ischemic renal injuries. RAGE represents an important factor in innate immunity against pathogens, but it also interacts with endogenous ligands, resulting in chronic inflammation. RAGE signaling has been implicated in multiple human illnesses, including atherosclerosis, arthritis, Alzheimer’s disease, atherosclerosis and aging associated diseases.

References and Literature :
1. Zhou Z,et al.(2011) RAGE and its ligands in bone metabolism. Front Biosci (Schol Ed). 3: 768-76. 2. Mosquera JA. (2010) Role of the receptor for advanced glycation end products (RAGE) in inflammation]. Invest Clin. 51(2): 257-68. 3. D’Agati V,et al.(2010) RAGE and the pathogenesis of chronic kidney disease. Nat Rev Nephrol. 6(6): 352-60.

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