BCMA/TNFRSF17 protein is fully biologically active when compared to standard. The ED50 as determined by its ability to inhibit APRIL-mediated proliferation of anti-IgM stimulated murine B cells is no less than 40 ng/ml, corresponding to a specific activity of > 2.5 x 10^4 IU/mg in the presence of 100 ng/ml human APRIL.
Source
E. coli
Protein/Peptide Type
Recombinant Protein
Gene
TNFRSF17
Purity
> 98 % pure by SDS-PAGE and HPLC
Endotoxin Note
Less than 1 EU/ug of BCMA/TNFRSF17 as determined by LAL method.
Applications/Dilutions
Dilutions
Bioactivity
SDS-Page
Theoretical MW
5.4 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.
Publications
Read Publication using NBP2-34903 in the following applications:
Store at -20 to -70C as supplied. After reconstitution, store at 2 to 8C for 1 month and at -20 to -70C for long term storage. Avoid repeated freeze-thaw cycles.
Buffer
Lyophilized from a 0.2 um filtered concentrated solution in 30 % acetonitrile, 0.1 % TFA.
Preservative
No Preservative
Concentration
LYOPH
Purity
> 98 % pure by SDS-PAGE and HPLC
Reconstitution Instructions
Recommended to centrifuge prior to opening. Reconstitute in sterile distilled water or aqueous buffer containing 0.1% BSA to a concentration of 0.1-1.0mg/mL. Apportion stock solutions into working aliquots and store at <-20C.
Notes
This lyophilized preparation is stable for 12 months from date of receipt at -20 to -70 degrees C, preferably desiccated. Upon reconstitution, the preparation can be stored for 1 month at 2-8 degrees C under sterile conditions, and for 3 months at -20 degrees C to -70 degrees C. Use a manual defrost freezer and avoid repeated freeze-thaw cycles. Stock solutions should be aliquoted and stored at < -20 degrees C. Further dilutions should be made in appropriate buffered solutions
Alternate Names for Recombinant Human BCMA/TNFRSF17 Protein
B cell maturation antigen
B-cell maturation protein
BCMA
BCMA/TNFRSF17
BCMAtumor necrosis factor receptor superfamily member 17
BCMB-cell maturation factor
CD269 antigen
CD269
TNFRSF13A
TNFRSF17
tumor necrosis factor receptor superfamily, member 17
Background
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
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Peptides and proteins are guaranteed for 3 months from date of receipt.
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