Recombinant Human Serpin A6 Protein, CF Summary
Product Specifications
Met23-Val405, with a C-terminal 6-His tag
Analysis
Product Datasheets
Carrier Free
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
9580-PI
Formulation | Lyophilized from a 0.2 μm filtered solution in Tris, NaCl and Trehalose. |
Reconstitution | Reconstitute at 1 mg/mL in water. |
Shipping | The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below. |
Stability & Storage: | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Scientific Data
When Cortisol-BSA Conjugate is immobilized at 5 μg/mL, 100 μL/well, Recombinant Human Serpin A6 (Catalog # 9580-PI) binds with an ED50 of 1.5-7.5 μg/mL.
Reconstitution Calculator
Background: Serpin A6
Corticosteroid-binding globulin (CBG), also known as Serpin A6, is an approximately 42 kDa member of the serpin superfamily of serine protease inhibitors. CBG belongs to the clade A subgroup of serpins which include inflammatory response molecules (1). Human CBG shares 57% sequence identity to mouse CBG. CBG is one of two serpins known to bind and transport hormones. CBG is responsible for binding ~90% of cortisol in a reversible manner to regulate levels under normal physiological states (2). However, cleavage of CBG's reactive site loop by proteases present during an inflammatory response leads to a targeted and immediate release of the anti-inflammatory steroid, cortisol, from CBG (3). Reduced cleavage of CBG is implicated in the inflammatory phenotype seen in obesity, metabolic syndrome, and rheumatoid arthritis (4, 5). Cleavage of CBG can be modulated by glycosylation (6). Naturally occurring mutations of CBG lead to abnormal levels or function (7, 8). Loss of functional CBG results in low cortisol levels in patients experiencing chronic pain, fatigue, hypotension and excess weight (8).
- Law, R. et al. (2006) Genome Biol. 7:216.
- Lewis, J. G. et al (2005) Clin. Chem. Acta. 359:189.
- Klieber M.A. et al. (2007) J. Biol. Chem. 282:29594.
- Nenke, M.A. et al. (2016) Horm. Metab. Res. 48:523.
- Nenke, M.A. et al. (2016) Clin. Endocrinol. 85:369.
- Sumer-Bayraktar, Z. et al. (2016) J. Biol. Chem 291:17727.
- Simard, M. et al. (2015) J. Clin. Endocrinol. Metab. 100:E129.
- Gagliardi, L. et al. (2010) Mol. Cell. Endocrinol. 316:24.
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