|CD236||GYPC (Glycophorin C)[Gerbich blood group]|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Lineage Restricted Molecule|
Type 3 glycoprotein
|40 / 40|
|CD236 is expressed on red cells, erythrocytes, erythroid cells and stem cell subsets. Expression is in a wide variety of tissue cells, such as kidney, thymus, stomach, breast and adult liver. It is expressed on non-erythroid cell lines are expressed but at a lower level and differentially glycosylated. CD236 expression is ubiquitous.|
|MOLECULAR FAMILY NAME: Belongs to the glycophorin family.|
CD236 is a single-pass type-3 glycoprotein. It contains an 57 aa extracellular domain which contains 14 O-linked and 1 N-linked glycosylation sites, a 24 aa transmembrane domain and a 47 aa intracellular cytoplasmic domain.
Alternative splicing yields 2 different isoforms.
POST-TRANSLATIONAL MODIFICATION: No information.
|LIGANDS AND MOLECULES ASSOCIATED WITH CD236|
P. falciparum erythrocyte binding protein 2 binds CD236.
|Together with membrane p55, CD236 is linked to the cytoskeletal protein band 4.1. This interaction assists in maintaining the mechanical stability and deformability of erythrocytes. The CD236 gene encodes the Gerbich blood group (Ge) and is closely related to sialoglycoproteins in the human red blood cell membrane. CD236 is one of the chored proteins of red blood cells skeleton that maintains cell morphology. CD236 antigens appear to be not essential for the viability of red cells. It is thought that CD236 is an abridged version of CD236R. Naturally occurring anti-Ge antibodies have been found but are not clinically significant. However antibodies to Ge antigens have been associated with transfusion reactions and mild hemolytic disease of the newborn. The Leach and Yussef phenotype is also due to a deletion on the gene. Individuals with the Leach phenotype are devoid of CD236 due to a deletion in CD236 gene and have erythrocytes that are elliptocytic and less deformable. Further more these individuals are less susceptible to infection with Plasmodium falciparum. No pathology is associated with this pheotype. The Yussef phenotype is due to a 57 base pair deletion in exon 2 of CD236. The Webb and Duch antigens, also known as CD236, result from single point mutations of CD236 gene. The rare Webb antigen arises from a base substitution at nucleotide 23, which results in insertion of an asparagine residue instead of a serine during protein synthesis and loss of a glycosylation site. The Duch antigen is the result to a C to T transition at neucine by phenylalanine.|
BIOCHEMICAL ACTIVITY: No information.
DISEASE RELEVANCE AND FUNCTION OF CD236 IN INTACT ANIMAL: No information.
|MOLECULAR INTERACTIONS -|
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CD236: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD236: No information.
Database accession numbers
Revised June 25, 2008