|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Recombinant Human SerpinA3 protein (Catalog#10307-H08H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human SerpinA3 (rh SerpinA3; Catalog#10307-H08H; NP_001076.2; Met 1-Ala 423). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.|
|Human SerpinA3 / SERPINA3|
No cross-reactivity in ELISA with
Human SerpinA1 / A1AT
Human SerpinA5 / PROCI
Human SerpinC1 / Antithrombin-III
Human SerpinD1 / HC2
Human SerpinF2 / AAP
Human cell lysate (293 cell line)
ELISA: 0.5-1 μg/mL
This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human SerpinA3. The detection limit for Human SerpinA3 is approximately 0.078 ng/well.
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Human SerpinA3, also known as Alpha 1-antichymotrypsin (AACT), is a plasma alpha globulin glycoprotein, and is a member of serpin superfamily of the serine protease inhibitors consisting of at least 35 members. SerpinA3 has been demonstrated to inhibit the activity of certain serine proteases, such as cathepsin G found in neutrophils, and chymases present in mast cells, by inducing a major conformational rearrangement, and thus protects some tissues from damage caused by proteolytic enzymes. This enzyme is produced primarily in the liver, and is identified as an acute-phase inflammatory protein. SerpinA3 deficiency has been associated with liver disease, and mutations of this gene have been observed in patients with Parkinson disease and chronic obstructive pulmonary disease. In addition, ACT gene polymorphism has been implicated with Alzheimer’s disease (AD), cerebral amyloid angiopathy (CAA), as well as stroke, since SerpinA3 is a major constituent of the plaques in AD and an inhibitor of amyloid beta peptide degradation.