|CD268||TNFRSF13C (tumor necrosis factor receptor, superfamily member 13C), BR3, BAFF-R|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Non-lineage Restricted Molecule|
Type 3 glycoprotein
|19 / 19|
25 / 25
|CD268 is expressed on B cells, peripheral blood lymphocytes and lymphoid tissue. There is a high expression in spleen, lymph node and circulating peripheral blood leukocytes. Expression is on resting B cells and on CD4+ T cells but is down regulated on activation.|
|MOLECULAR FAMILY NAME: Belongs to the tumor necrosis receptor family.|
CD268 is a single-pass type-3 172 aa glycoprotein. It contains an extracellular domain which contains 1 N-glycosylation site in the murine molecule, which is absent from the human sequence, and 4 cysteine-rich domains which is fewer than in typical TNFR family members which contain 6 or more cysteines, a transmembrane domain and a 25 aa cytoplasmic domain which contains a 25 aa C-terminus that is probably involved in signal transduction.
POST TRANSCRIPTIONAL MODIFICATION
Alternative splicing yields 2 different isoforms.
POST-TRANSLATIONAL MODIFICATION: No information.
|LIGANDS AND MOLECULE ASSOCIATED WITH CD268|
CD268 is one of several receptors that bind the TNF family member CD257 (BAFF).
|The physiological function of CD268 is not yet clear. CD268 is a B cell activating factor specific for CD257. CD268 is one of three known receptors namely CD268 (BAFF-R), CD269 (BCMA) and CD267 (TACI). Unlike CD269 and CD267, CD268 does not bind CD256 (APRIL). The CD268 knockout mice interaction, in vitro, is thought to have important implications to be the principle receptor for B cell development, maturation and survival but which receptor is responsible is not clear. The knockout mice have not been analyzed but a natural mutation in the CD268 intracellular domain in mice is associated with apparently normal B cell precursors but fewer mature B cells. B cells from these mice do not respond to CD268, whereas mice lacking the other two receptors have normal numbers of mature B cells, indicating it is CD268 that mediates the effects of CD257 on mature B cell survival.|
BIOCHEMICAL ACTIVITY: No information.
DISEASE RELEVANCE AND FUNCTION OF CD268 IN INTACT ANIMAL
The role of CD257 in B cell survival and activation make CD268 a potential diagnostic reagent. Elevated levels are associated with autoimmune diseases and CD268 or its receptors are the potential targets for therapy of autoimmune disease. Experimental administration of a CD268 Fc fusion suppresses antibody responses. CD268 may aslo be involved in survival B cell malignancies. Overexpression of CD268 in mice results in mature B cell hyperplasia and symptoms of systemic lupus erythematosus (SLE). Some SLE patients have increased levels of CD268 in serum, therefore it has been proposed that these abnormally high levels may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells.
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CD268: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD268: No information.
For further information see Thompson, J.S. et al (2001) Science 293:2108-2111.
Database accession numbers
Revised June 25, 2008