CD268(BAFFR)-muIg Biotinylated

The human B cell activating factor (BAFF) and APRIL(a proliferation inducing ligand) are both type II molecules belonging to the TNF superfamily. They are expressed by non-B cells, and are down regulated by mitogenic stimulation(2).  BAFF and APRIL bind to at least two receptors: TACI (transmembrane activator and CAML-interactor) and BCMA (B cell maturation antigen), both of which are restricted to B cells(3,4).  Ligation of these receptors with recombinant BAFF dramatically increases IgM production by peripheral blood B cells(1).  A third receptor  for BAFF (BAFF-R) has been described(5). BAFF and BAFFR knockout mice have a reduced numbers of mature B cells in the periphery, however TACI and BCMA knockouts do not share this phenotype, suggesting that BAFF-R may the primary receptor for BAFF in mice(8,9,10).  Cell surface BAFF can be proteolytically cleaved to form a soluble trimeric molecule(2). Levels of soluble BAFF correspond with levels of autoantibodies in Sjogren’s Syndrome(11).  Recombinant human BAFFR-muIg binds to recombinant BAFF-muCD8 and can inhibit binding of this molecule to receptors on Raji cells.

Molecular Structure:  A soluble molecule consisting of the extracellular (60aa) domain of human BAFFR fused  to the  murine IgG2a Fc (232 aa).  Predicted non glycosylated monomeric weight:  33.5 kd.

Murine CD8alpha leader:  kpqapelrgs  

linker: gs   

BAFFR (EC): rgprslrgrdapaptpcvpaecfdllvrhcvacgllrtprpkpagassppprtal     

linker: gt

Murine IgG2a Fc + hinge: eprgptikpcppckcpapnllggpsvfifppkikdvlmislspivtcvvvdvseddpdvqiswfvnnvevhtaqtqthredynstlrvvsalpiqhqdwmsgkefkckvnnkdlpapiertiskpkgsvrapqvyvlpppeeemtkkqvtltcmvtdfmpediyvewtnngktelnykntepvldsdgsyfmysklrvekknwvernsyscsvvheglhnhhttksfsrtpgk

Transfectant Cell Line:  CHO

Functional Application:  BAFFR-muIg binds to recombinant BAFF-muCD8 and can inhibit this molecule’s abiltiy to bind to receptors on Raji cells.

References:

1) Schneider P., J. Tschopp, et al. J. Exp. Med. 1999, 189(11):1747-1756.

2) Shu, H.B., H. Johnson, W.H. Hui. J Leukoc Biol 1999, 65:680-683.

3) Marsters, S.A., A. Ashkenazi, et al. 2000, Curr Biol 10:785-788.

4) Xia, X., H. Hsu, et al. 2000, J Exp Med, 192(1): 137-143.

5) Thompson J.S., C. Ambrose, et al. Science 2001, 293: 2108-2111.

6)Roschke,V, T.S. Migone, et al. J Immunol . 2002, 169: 4314-4321.

7) MacLennan, C.M., C.G. Vinuesa, 2002, Immunity 17:235-238.

8) B. Schiemann, et al, (2001) Science 293: 2111-2114.

9) S.M. Harless,et al, (2001) Curr Biol 11: 1988-1989.

10) Mol Cell Biol (2001) 21: 4067-4074.

11) X. Mariette, et al, (2003) Ann Rhem Dis 62: 168-171.