Reactivity | HuSpecies Glossary |
Applications | Binding Activity |
Format | Carrier-Free |
Details of Functionality | Measured by its ability to bind biotinylated rhBLAME in a functional ELISA. |
Source | Mouse myeloma cell line, NS0-derived human BLAME/SLAMF8 protein Ala23-Asp233, with a C-terminal 6-His tag |
Accession # | |
N-terminal Sequence | Ala23 |
Protein/Peptide Type | Recombinant Proteins |
Gene | SLAMF8 |
Purity | >90%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Endotoxin Note | <0.10 EU per 1 μg of the protein by the LAL method. |
Dilutions |
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Theoretical MW | 24.7 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
SDS-PAGE | 30 - 40 kDa, reducing conditions |
Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
|
Buffer | Lyophilized from a 0.2 μm filtered solution in Sodium Citrate and NaCl. |
Purity | >90%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Reconstitution Instructions | Reconstitute at 100 μg/mL in sterile PBS. |
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).
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