• Purity

  >95%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.01 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its ability to inhibit BAFF-mediated proliferation of anti-IgM stimulated mouse B cells. Moore, P.A.     et al. (1999) Science     285:260; Gross, J.A.     et al. (2000) Nature     404:995; Schneider, P.     et al. (1999) J. Exp. Med.     189:1747. The ED    ₅₀ for this effect is 20-80 ng/mL in the presence of 5 ng/mL recombinant human BAFF.

• Source

  Mouse myeloma cell line, NS0-derived

  Human BAFF R (Ser7-Ala71) Accession # Q96RJ3	DIEGRMD	Human IgG1 (Pro100-Lys330)
  N-terminus		C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Starts at Ser7

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  33 kDa (monomer)

• SDS-PAGE

  40-50 kDa, reducing conditions

Background: BAFF R/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.

• References:

1. Rolink, A.G. and F. Melcher (2002) Curr. Opin. Immunol. 14:266.

2. Mackay F. and J.L. Browning (2002) Nature Reviews Immunology 2:464.

3. Laabi, Y. et al. (2001) Current Biol. 11:R1013.

4. Thompson, J.S. et al. (2001) Science 14:2108.

• Long Name:

  B cell Activating Factor Receptor

• Entrez Gene IDs:

  115650 (Human); 72049 (Mouse)

• Alternate Names:

  BAFF R; BAFFR; BR3; CD268; TNFRSF13C