More info
Assay range | 3.12-200 ng/ml |
Sensitivity | 3.0 ng/ml |
Specificity | No cross-reaction with other related substances detected |
Size | 96T |
Storage | Store at 2 - 8ºC. Keep reconstituted standard and detection Ab at -20 ºC |
Assay Principle | Sanwich ELISA |
Sample Volume | 50 µL final volume, dilution factor varies on samples |
Sample Type | plasma, serum, milk, urine, CSF and cell culture supernatants |
Detection Method | Chromogenic |
Kit Components
1. Recombinant Human AHSG standard: 1 vial
2. One 96-well plate coated withHuman AHSG Ab
3. Diluent buffer (10x): 30 mL - 1
4. Biotinylated Human AHSG Ab (50x): 1 40 µL
5. Streptavidin-HRP(100x): 80 µL
6. TMB developing agent: 8 mL x1
7. Stop solution: 12 mL x1
8. Washing solution (20x): 30 mL x2
Background
Human Fetuin A, also known as α2-Heremans-Schmid glycoprotein (AHSG), Alpha-2-Z-globulin, or Ba-alpha-2-glycoprotein, is a member of the cystatin superfamily. Fetuin A is mainly produced by hepatocytes and monocytes/macrophages and is most abundant in the plasma and in the bone. In the plasma, Fetuin A is a disulfide bond-linked two chain polypeptide consisting of two N-terminal cystatin domains and a smaller C-terminal domain. In the bone, Fetuin A is the most abundant non-collagenous protein. It accumulates in the bone through strong binding to apatite. Fetuin-A forms soluble complexes with calcium and phosphate and thus is a carrier of insoluble calcium phosphate. It is reported that purified bovine Fetuin A, when added into a solution supersaturated with calcium phosphate, is able to inhibit the precipitation of calcium phosphate mineral. Thus fetuin-A is a potent inhibitor of pathological calcification. Gene knockout mice bearing no Fetuin A protein have increased risk for etopic calcification in blood vessels. In addition, it has been shown that serum levels of Fetuin A are significantly lower in end stage renal failure patients on long-term hemodialysis than in healthy controls. Sera from these patients show an impaired capacity to inhibit calcium phosphate precipitation. This impairment is corrected when purified Fetuin A is added. Therefore, decreased serum Fetuin A levels may contribute to accelerated vascular calcification in uremic patients. It is proposed that Fetuin A serum levels may be a useful biomarker to predict artery calcification and mortalities in renal failure patients. Recently, it has been shown that Fetuin A may play a role in endocytosis, brain development and the formation of bone tissue.