|CD262||TNFRSF10b (tumor necrosis factor receptor superfamily, member b), TRAIL-R2, DR5|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Non-lineage Restricted Molecule|
Type 1 glycoprotein
|48 / 48|
|CD262 expression is broad. Expression is wide in adult and fetal tissues and high in tumor cell lines. High expression is in lymphoid tissue, lung, peripheral blood leukocytes, pancreas, spleen, thymus, prostate, ovary, heart, placenta, uterus, testis, esophagus, stomach, intestine and liver but is not detected in the brain. Expression is induced by tumor suppressor p53. |
|MOLECULE FAMILY NAME: Belongs to the tumor necrosis factor receptor superfamily.|
CD262 is a single-pass type-1 440 aa glycoprotein. It contains 55 signal sequence, an 155 aa extracellular domain containing 3 TNFR cysteine-rich repeats but lacks N-glycosylation sites, a 21 aa transmembrane domain and a 209 cytoplasmic domain which contains an intracellular death domain.
Alternative splicing yields 2 different isoforms.
POST-TRANSLATIONAL MODIFICATION: No information.
|LIGANDS AND MOLECULE ASSOCATED WITH CD262|
CD262 binds to CD253 (TRAIL, TNFS10).
|CD262 acts as a ligand for CD253 (TRAIL) and contains a cytoplasmic death domain, which mediates the apoptosis of sensitive cells via the adaptor molecule FADD and caspase-8. The receptor can be activated by tumor necrosis factor-related apoptosis inducing ligand CD253 and transduces apoptosis signal. Studies with FADD-deficient mice suggested that FADD, a death domain containing adaptor protein, is required for the apoptosis mediated by this protein and FADD recruits caspase-8 to the activated receptor. Activation of NF-κB is promoted. CD262 is regulated by the tumor suppressor p53. |
BIOCHEMICAL ACTIVITY: No information.
DISEASE RELEVANCE AND FUNCTION OF CD262 IN INTACT ANIMAL
Defects in CD262 may be a cause of squamous cell carcinoma of the head and neck.
PROTEIN AND DNA ELEMENTS WHICH REGULATE TRANSCIPTION OF CD262: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD262: No information.
For further information see Griffith, T. S. et al (1999) J. Immunol. 162: 2597-2605.
Database accession numbers
Revised June 25, 2008