Mouse BAFFR/TNFRSF13C Alexa Fluor® 350-conjugated Antibody

Applications

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Preparation and Storage

Background: BAFFR/TNFRSF13C

B-cell activating factor (BAFF), also known as BlyS, TALL-1, TNAK, and zTNF4, is a TNF ligand superfamily member and has been designated TNFSF13B. It is produced by macrophages, dendritic cells, and T lymphocytes. BAFF promotes the survival of B cells and is essential for B cell maturation (1 - 4). BAFF binds to three TNF receptor superfamily members: B-cell maturation antigen (BCMA/TNFRSF17), transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF R/BR3/TNFRSF 13C). These receptors are type III transmembrane proteins that lack a signal peptide. Whereas TACI and BCMA bind BAFF and another TNF superfamily ligand, APRIL(a proliferation-inducing ligand), BAFF-R selectively binds BAFF. Mouse BAFF-R cDNA encodes a 175 amino acid residue (aa) transmembrane protein with a 71 aa extracellular domain, a 21 aa transmembrane domain, and a 83 aa cytoplasmic region. A second isoform of BAFF R that has a 72 aa cytoplamic region can also be produced by alternative splicing. The BAFF R extracellular domain lacks the TNF receptor canonical cysteine-rich domain (CRD) and contains only a partial CRD with four cysteine residues. Human and mouse BAFF R share 56% aa sequence identity. BAFF R is highly expressed in spleen, lymph node and resting B cells. It is also expressed at lower levels in activated B cells, in resting CD4⁺ T cells, in thymus and peripheral blood leukocytes. BAFF knockout mice lack mature B cells and has profound defects in antibody mediated immune responses. Similarly, A/WySnJ mice that are defective in BAFF R intracellular signaling also lack mature B cells, suggesting that BAFF R is the critical receptor for BAFF during B lymphopoiesis. In contrast, BCMA- or TACI-deficient mice have no major defect in B-cell development. While the function of BCMA is not defined, TACI has been shown to control B-cell homeostasis and T-cell-independent immune responses.

Product Datasheets

Related Research Areas

• B Cell Development and Differentiation
• Co-stimulatory and Co-inhibitory Molecules
• Regulation of Apoptosis by TNF Superfamily Members
• Regulation of B Cell Activation and Homeostasis by TNF Superfamily Members
• Regulation of T Cell Co-stimulation by TNF Superfamily Members
• TNF Superfamily
• TNF Superfamily Receptors