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

B Cell Maturation Antigen (BCMA) also referred to as TNFRSF17 or CD269, is a transmembrane glycoprotein member of the tumor necrosis factor receptor (TNFR) superfamily. BCMA is used as a biomarker for Multiple myeloma (MM). BCMA mainly plays an important role in B cells for their proliferation, survival and also differentiates them into plasma cells^[1]. BCMA/TNFRSF17 Protein, Human (HEK293, His-Avi) is a recombinant protein with a C-Terminal Avi label and a C-Terminal His label, It consists of 54 amino acids (M1-A54) and is produced in HEK293 cells.

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

BCMA (human; 1 µg; i.p.; on days -4, -2, , 2, and 4) decreases the IgA and IgM levels in C57 Bl/6 mice^[4].

Human

HEK293

C-Avi;C-His

Q02223 (M1-A54)

608  [NCBI]

Approximately 12 kDa & 15-17 kDa

Greater than 95% as determined by Tris-Bis PAGE.

<1 EU/μg, determined by LAL method.

• [1]. Nobari ST, et al. B-cell maturation antigen targeting strategies in multiple myeloma treatment, advantages and disadvantages. J Transl Med. 2022 Feb 10;20(1):82.  [Content Brief]

  [2]. Yu B, et al. BCMA-targeted immunotherapy for multiple myeloma. J Hematol Oncol. 2020 Sep 17;13(1):125.  [Content Brief]

  [3]. Perez-Amill L, et al. Preclinical development of a humanized chimeric antigen receptor against B cell maturation antigen for multiple myeloma. Haematologica. 2021 Jan 1;106(1):173-184.  [Content Brief]

  [4]. Sanchez E, et al. Soluble B-Cell Maturation Antigen Mediates Tumor-Induced Immune Deficiency in Multiple Myeloma. Clin Cancer Res. 2016 Jul 1;22(13):3383-97.  [Content Brief]

  [5]. O'Connor BP, et al. BCMA is essential for the survival of long-lived bone marrow plasma cells. J Exp Med. 2004 Jan 5;199(1):91-8.  [Content Brief]

  [6]. Tai YT, et al. APRIL and BCMA promote human multiple myeloma growth and immunosuppression in the bone marrow microenvironment. Blood. 2016 Jun 23;127(25):3225-36.  [Content Brief]