Human BAFFR/TNFRSF13C APC-conjugated Antibody Summary
Arg2-Ala71
Accession # Q96RJ3
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.
Scientific Data
Detection of BAFF R/TNFRSF13C in Human PBMCs by Flow Cytometry. Human peripheral blood mononuclear cells (PBMCs) were stained with Mouse Anti-Human CD19 PE-conjugated Monoclonal Antibody (Catalog # FAB4867P) and either (A) Goat Anti-Human BAFF R/TNFRSF13C APC-conjugated Antigen Affinity-purified Polyclonal Antibody (Catalog # FAB1162A) or (B) Normal Goat IgG Allophycocyanin Control (Catalog # IC108A). View our protocol for Staining Membrane-associated Proteins.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
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. 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/TNFRSF13C). 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. 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 cell, in resting CD4+ T cells, in thymus and peripheral blood leukocytes. BAFF knockout mice lack mature B cells. 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.
- Rolink, A.G. and F. Melcher (2002) Curr. Opin. Immunol. 14:266.
- Mackay F. and J.L. Browning (2002) Nature Reviews Immunology 2:464.
- Laabi, Y. et al. (2001) Current Biol. 11:R1013.
- Thompson, J.S. et al. (2001) Science 14:2108.
Product Datasheets
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