|CD269||TNFRSF17 (tumor necrosis factor receptor superfamily, member 17), BCMA, BCM|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Non-lineage Restricted Molecule|
Type 3 glycoprotein
|27 / 27|
|CD269 is expressed in mature and perinuclear B cells and plasma cells, plasmablasts and tonsillar germinal center B cells but not in T cells or monocytes. CD269 has low surface density and most remains intracellular where it is associated with peri-nuclear Golgi-like structures.|
|MOLECULAR FAMILY NAME: Belongs to the tumor necrosis factor receptor family.|
CD269 is a single-pass type-3 184 aa glycoprotein. It contains a 23 aa signal sequence, a 54 aa extracellular domain which contains a TNFR Cys repeat, a transmembrane domain and a 107 aa cytoplasmic domain which has a conserved motif of 6 cysteines in the N-terminal region and TRAFs1, 2, 3, 5 and 6.
POST-TRANSCRIPTIONAL MODIFICATION: No information.
POST-TRANSLATIONAL MODIFICATION: No information.
|LIGANDS AND MOLECULES ASSOCIATED WITH CD269|
CD269 binds CD257 (TALL1) with low affinity and CD256 (TALL2) with high affinity.
|CD269 like CD267 (TACI), binds CD268 (BAFF) and CD256 (APRIL) promoting the differentiation and proliferation of B cells as well as B cell survival and autoimmune response and plays a role in the regulation of humoral immunity. It is shown to bind to CD257 (TNFSF13b) and to mediate signaling leading to NF-κB and JNK activiation. This receptor also binds various TRAF family members. CD269 is essential for plasma cell survival and long-lived bone marrow plasma cells. CD269-/- mice have normal serum Ig levels ande normal antibody responses but reduced numbers of long-lived bone marrow plasma cells compared to wild-type mice.|
BIOCHEMICAL ACTIVITY: No information.
DISEASE RELEVANCE AND FUNCTION OF CD269 IN INTACT ANIMAL
CD269 is a potential therapeutic target for selective elimination of plasma cells in the treatment of antibody-mediated autoimmunity. A chromosomal aberration involving CD269 is found in a form of T cell acute lymphoblastic leukemia (T-ALL) involves a translocation with IL-2 gene.
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CD269: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD269: No information.
For further information see Madry, C. et al (1998) Int. Immunol. 10: 1693-1702.
Database accession numbers
Revised June 25, 2008