|CD162R|| PEN5(post-translational modification of PSGL-1)|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Non-lineage Restricted Molecule|
Type 1 glycoprotein
|110 / 110|
140 / 140
220 / 220
240 / 240
|CD162R is expressed on CD56dim CD16+ NK cells, a subset of oligodendrogliomas, oligodendrocyte precursor cells and is probably involved in the migration of this transient and highly mobile cell population during fetal brain development. Expression is also on lymphocytes, myeloid cells and all pilocytic astrocytomas.|
|MOLECULAR FAMILY NAME: Belongs to the carbohydrate family.|
CD162R is an unusual poly-N-lactosame carbohydrate related to keratan sulphate glycosaminiglycans. At the surface of NK cells, CD162R glycoproteins are extended rod structures. CD162R is the high affinity counter-receptor for P-selectin on myeloid cells and stimulated T lymphocytes. As such, it plays a critical role in the tethering of these cells to activated platelets or endothelia expressing P-selectin. The organization of the CD162R gene closely resembles that of CD43 and the human platelet glycoprotein Gplb-a, both of which have an intron in the 5-prime-non-coding region, a long 2nd exon containing the complete coding region, and TATA-less promoters. This sulfated lactosamine epitope creates an unique binding site for L-selectin (CD62L), independent of tyrosine sulfation.
MOLECULAR MASS: No information.
POST-TRANSCRIPTIONAL MODIFICATION: No information.
The CD162R is a post-translational modification of P-selectin ligand 1 (CD162). It is a developmentally regulated marker of both immune and neural cells.
|LIGANDS AND MOLECULES ASSOCIATED WITH CD162R|
CD162R binds CD62L.
|The CD162R epitope creates an unique binding site for L-selectin which is independent of the CD162 tyrosine sulfation. CD162R acts as a trafficking and homing receptor for NK cells as it promotes NK cell tethering and rolling on inflammed endothelium as well as leukocyte-leukocyte interaction at sites of inflammation. On the surface of NK cells, the expression of CD162R is co-ordinated with the disappearance of L-selectin and the upregulation of killer cell Ig-like receptors, KIR. Therefore NK cell differentiation is accompanied by the acquisition of the CD162R carbohydrate decorating CD162. It is postulated that CD162R can serve as part of a combination code to deliver KIR+ NK cells to specific tissues.|
BIOCHEMICAL ACTIVITY: No information.
DISEASE RELEVANCE AND FUNCTION OF CD162R IN INTACT ANIMAL
CD162R is a special marker for NK cells and oligodendrocyte precursor cells. The surface expression of CD162R is down moduated by stimuli that induce NK cell proliferation. It is absent from leukemic NK cells of patients with aggressive granular lymphocyte proliferative disorder. In human central nervous system tumors, CD162R has been observed in a subset of oligodendrocyte precursor cells which probably is involved in the migration of this transient and highly mobile cell population during fetal brain development. Its protein carrier is CD162. The data suggest that CD162R is a useful developmentally regulated marker shared by cells belonging to immune and neural systems and is a marker in the diagnosis of pilocytic astrocytomas.
| MOLECULAR INTERACTIONS -|
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CD162R: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD162R: No information.
Database accession numbers
Revised June 25, 2008