Recombinant Human BLAME/SLAMF8 Protein, CF Summary
Ala23-Asp233, with a C-terminal 6-His tag
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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.
|Formulation||Lyophilized from a 0.2 μm filtered solution in Sodium Citrate and NaCl.|
|Reconstitution||Reconstitute at 100 μg/mL in sterile PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
BLAME (B-lymphocyte activator macrophage expressed), also known as SLAM family member 8, is a type I transmembrane protein that belongs to the CD2 subset of immunoglobulin superfamily cell receptors. CD2 family proteins function as adhesion molecules and modulators of immune responses (1, 2). Mature human BLAME consists of a 211 amino acid (aa) ECD that contains two Ig V-like domains, a 21 aa transmembrane segment, and a 31 aa cytoplasmic tail that lacks recognizable signaling motifs (3). Within the ECD, human BLAME shares 19% - 26% aa sequence identity with human 2B4, CD2, CD2F-10, CD48, CD58, CD84, CD229, CRACC, NTB-A, and SLAM. It shares 79% aa sequence identity with the ECD of mouse BLAME. BLAME is expressed on dendritic cells and IFN-gamma stimulated monocytes. Overexpression of BLAME in bone marrow cells leads to an increase in the peritoneal B1b population of B lymphocytes (3).
- McNerney, M.E. and V. Kumar (2006) Curr. Top. Microbiol. Immunol. 298:91.
- Veillette, A. (2006) Nat. Rev. Immunol. 6:56.
- Kingsbury, G.A. et al. (2001) J. Immunol. 166:5675.
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