BCMA/TNFRSF17 Overexpression Lysate

HEK293T cells in 10-cm dishes were transiently transfected with a non-lipid polymer transfection reagent specially designed and manufactured for large volume DNA transfection. Transfected cells were cultured for 48hrs before collection. The cells were lysed in modified RIPA buffer (25mM Tris-HCl pH7.6, 150mM NaCl, 1% NP-40, 1mM EDTA, 1xProteinase inhibitor cocktail mix, 1mM PMSF and 1mM Na3VO4, and then centrifuged to clarify the lysate. Protein concentration was measured by BCA protein assay kit.This product is manufactured by and sold under license from OriGene Technologies and its use is limited solely for research purposes.

B cell maturation antigen (BCMA), also known as tumor necrosis factor receptor superfamily member 17 (TNFRSF17), is a type III transmembrane glycoprotein that plays a role in B cell maturation and differentiation into plasma cells and is a therapeutic target for treatment of multiple myeloma (MM) (1,2). BMCA is synthesized as a protein of 184 amino acids (aa) in length with a theoretical molecular weight of 20.2 kDa consisting of an extracellular N-terminus containing 6 cysteine residues, a transmembrane domain, and an intracellular tumor necrosis factor (TRAF) binding domain (1). BCMA is functionally similar to two other TNFR superfamily members, B cell activation factor receptor (BAFF-R) and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) (1,2). BCMA is primarily expressed on plasmablasts, plasma cells, and late-stage B cells (1,2).

BCMA has two agonistic ligands: BAFF and a proliferation-inducing ligand (APRIL) (1,2). APRIL has higher affinity for BCMA than BAFF and the binding is mediated by CD138/syndeclin-1 (2,3). Activation of BCMA promotes the growth and survival of plasma cells, or MM cells in disease, through several signaling pathways such as NFkappaB, MEK/ERK, AKT, JNK, and p38 (1,2). In MM cells the BCMA activation and downstream signaling cascade functions to upregulate antiapoptotic proteins including Bcl-2, Bcl-xL, and Mcl-1 and protect the cells against therapeutic agents like dexamethasone (2,3).

Given its specific expression on plasma cells but not memory B cells, naive B cells, or hematopoietic stem cells, BCMA has garnered much interest as a therapeutic target for the treatment of MM (1-4). Current BCMA-targeted immunotherapy strategies include antibody-drug conjugates (ADC), chimeric antigen receptor (CAR) T cells, bispecific T cell engager (BiTE), and bispecific/trispecific antibodies (1-4). CAR T cell therapy in particular has demonstrated promising clinical results (2,4). Still, more research needs to be done to improve the efficacy and risk of relapse following CAR T cell therapy and may also include targeting additional antigens in combination with BCMA or utilizing pharmacological agents to increase antigen density (4).

References

1. Yu, B., Jiang, T., & Liu, D. (2020). BCMA-targeted immunotherapy for multiple myeloma. Journal of hematology & oncology, 13(1), 125. https://doi.org/10.1186/s13045-020-00962-7

2. Cho, S. F., Anderson, K. C., & Tai, Y. T. (2018). Targeting B Cell Maturation Antigen (BCMA) in Multiple Myeloma: Potential Uses of BCMA-Based Immunotherapy. Frontiers in immunology, 9, 1821. https://doi.org/10.3389/fimmu.2018.01821

3. Dalla Palma, B., Marchica, V., Catarozzo, M. T., Giuliani, N., & Accardi, F. (2020). Monoclonal and Bispecific Anti-BCMA Antibodies in Multiple Myeloma. Journal of clinical medicine, 9(9), 3022. https://doi.org/10.3390/jcm9093022

4. Mikkilineni, L., & Kochenderfer, J. N. (2021). CAR T cell therapies for patients with multiple myeloma. Nature reviews. Clinical oncology, 18(2), 71-84. https://doi.org/10.1038/s41571-020-0427-6

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Lysates are guaranteed for 6 months from date of receipt.

Array NBL1-17151

• BCMA/TNFRSF17 Antibodies
• BCMA/TNFRSF17 Lysate
• BCMA/TNFRSF17 Proteins
• BCMA/TNFRSF17 ELISAs
• BCMA/TNFRSF17 Proteins and Enzymes