We recommend to avoid using bovine serum albumin (BSA) as a buffer component or blocking agent for SAA immunoassay. In buffers, BSA can be replaced with 1% casein. When developing an SAA immunoassay in microtiter plates, it is important to prevent non-specific binding of SAA to the wells of a plate. Plates blocking procedure and antigen dilution buffer should be optimized to ensure that SAA non-specific binding to the plate wells is suppressed. Buffer containing 1% casein and 0.05% Tween 20 is suggested for recommended MAb combinations.
Publications
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The serum amyloid A (SAA) family comprises a number of differentially expressed lipoproteins, acute phase SAA1 and SAA2, the former being a major component in plasma, and constitutive SAA's (C-SAAs). Although the liver is the primary site of synthesis of both SAA types, extrhepatic production has been reported. The in vivo concentrations increase by as much as 1000 fold during inflammation. Several studies have expressed it's importance in the diagnosis and monitoring of various diseases. Pathological SAA values are often detected in association with normal CRP concentrations. SAA rises earlier and more sharply than CRP. SAA enhances the binding of HDL's to macrophages and thus helps the delivery of lipid to sites of injury for use in tissue repair. It is thus thought to be an integral part of the disease process. In addition, recent experiments suggest that SAA may play a "housekeeping" role in normal human tissues. Elevated levels of SAA over time predispose secondary amyloidosis, extracellular accumulation of amyloid fibrils, derived from a circulating precursor, in various tissues and organs. The most common form of amyloidosis occurs secondary to chronic inflammatory disease, particularly rheumatoid arthritis.
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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