BCMA/TNFRSF17 Trimer Protein, Human (Biotinylated, HEK293, His-Avi)

BCMA is expressed preferentially by mature B lymphocytes, with minimal expression in hematopoietic stem cells or nonhematopoietic tissue^[1]. BCMA is almost exclusively expressed on plasmablasts and PCs^[2].
The amino acid sequence of human BCMA protein has low homology for mouse BCMA protein.
BCMA is a 184 amino acid and 20.2-kDa type III transmembrane glycoprotein, with the extracellular N terminus containing a conserved motif of 6 cysteines. BCMA has two agonist ligands: a proliferation-inducing ligand (APRIL) and B cell activating factor (BAFF). Upon binding of the ligands to BCMA, activates B cells (NF-κβ), rat sarcoma/mitogen-activated protein kinase (RAS/MAPK), and phosphoinositide-3-kinase-protein kinase B/Akt (PI3K-PKB/Akt) signaling pathway. These pathways result in proliferation stimulation by modulating cell cycle checkpoints, increasing survival by upregulating anti-apoptotic proteins, and production of cell adhesion molecules, angiogenesis factors, and immunosuppressive molecules^[2].
BCMA can be used as a promising antigen to target using a variety of immuno-therapy treatments including CART cells, for MM patients^[3]. BCMA markedly reduces plasma IgA, IgG, and IgM levels and splenic Ig heavy chain mRNA levels in mouse^[4]. In BCMA−/− mice, the long-term survival of PCs is impaired, but lack of BCMA has no effect in short-lived PCs, B cell development, or early humoral immune response, and the splenic architecture and germinal centers appear intact in these BCMA-deficient mice^[5]. BCMA overexpression significantly promotes in vivo growth of xenografted MM cells in murine models^[6].

BCMA (human; 10000 ng/mL; 24 h) blocks the activity of ARI2m cells and inhibits the IFNγ production^[3].

BCMA (human; 100 µg; i.p.; on days -4, -2, 0, 2, and 4) decreases the IgA and IgM levels in C57 Bl/6 mice^[4].