BAFFR (BAFF receptor) is one of the three receptors recognized by BAFF. The other two are BCMA and TACI which also interact with APRIL. April does not interact with BAFFR. All three receptor of BAFF are type III membrane proteins that do not contain signal peptides.
Interacting protein(s): BAFF (P7003M)
Related products: TNF-Receptor Superfamily
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Quick Specs
| Species: | Human |
| Catalog no.: | P7114G |
| Synonym: | CD268, BROMIX, TNFRSF13C, CVID4, prolixin |
| Tag: | Mouse IgG2a Fc, aglycosylated |
| GenBank accession: | NM_052945 |
| SwissPro accession: | Q96RJ3 |
| Expression host: | 293T |
| Construction: | Human BAFFR (R2-A70 with V20N/L27P mutations)-mouse IgG2a Fc, aglycosylated |
| MW (calculated): | 34,174 daltons |
| MW (SDS-PAGE): | 35 Kd |
| Abs 0.1% (= 1 mg/ml): | 0.967 |
| Purity: | 95 % |
Description
BAFFR (BAFF receptor) is one of the three receptors recognized by BAFF. The other two are BCMA and TACI which also interact with APRIL. April does not interact with BAFFR. All three receptor of BAFF are type III membrane proteins that do not contain signal peptides. The CRD (cysteine-rich domain) of BAFFR contains only 4 cysteine residues and is one of the smallest members of the TNF receptor superfamily (TNFRSF) (the other one is BCMA). As such it did not get identified as a TNFRSF member using by TNFR-directly database search. Rather, it was identified in BJAB (a human B cell line) does not express BCAM and TACI (two known receptors for BAFF at the time).
Among the gene-deficient mice of the 3 BAFF receptors, BAFFR(-/-) mice exhibit a phenotype that B cells fail to progress from transitional type 1 (T1) to transitional type 2 (T2). The T1/T2 blockade is also observed in BAFF (-/-) mice indicating that among the three receptors, BAFFR is probably the most critical for survival and transition of B cells. Unlike BCMA and TACI, ligation of BAFFR leads to activation of the alternative NFkB pathway. BAFF was first implicated for autoimmune diseases by BAFF transgenic mice.
In these mice B lymphoplasia and hyperglobulinemia is accompanied by production of autoantibodies and the development of glomerulonephritis as well as destruction of salivary gland tissues. BAFFR is an attractive therapeutic target for autoimmune disorders.
Amino Acid Sequence.
References
1. Schweighoffer E, Tybulewicz VL. BAFF signaling in health and disease. Curr Opin Immunol. 2021;71:124-31. Epub 20210802. doi: 10.1016/j.coi.2021.06.014. PubMed PMID: 34352467.
2. Mackay F, Woodcock SA, Lawton P, Ambrose C, Baetscher M, et al. (1999) Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations. J Exp Med. 190:1697-1710.
3. Thompson JS, Bixler SA, Qian F, Vora K, Scott ML, et al. (2001) BAFF-R, a newly identified TNF receptor that specifically interacts with BAFF. Science. 293:2108-2111.
4. Groom J, Kalled SL, Cutler AH, Olson C, Woodcock SA, et al. (2002) Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome. J Clin Invest. 109:59-68.
5. Pelletier M, Thompson JS, Qian F, Bixler SA, Gong D, Cachero T, Gilbride K, Day E, Zafari M, Benjamin C, Gorelik L, Whitty A, Kalled SL, Ambrose C, Hsu YM. (2003) J Biol Chem. 278:33127-33133