CLEC5A CLEC5A (C-type lectin domain family, 5)
Molecule TypeAntigen ExpressionMolecular Weight
Min / Max
Non-lineage Restricted Molecule
Type 2 glycoprotein
Monocyte
Macrophage
Peripheral blood

Expression
CLEC5A is expressed in peripheral blood monocytes, in monocyte/macrophage cell lines U937 and MonoMac6 but not in cell lines of other origins.  Expression is down regulated when monocytes differentiate into dendritic cells.

Structure
MOLECULAR FAMILY NAME: Belongs to the C-type lectin superfamily.

CLEC5A is a single-pass type-2 187 aa glycoprotein.  It contains an extracellular domain which contains a C-type lectin domain and a putative N-linked glycosylation site, a transmembrane domain which contains a positively charged amino acid that enables it to pair with dnax-activation protein 12 (Dap12) and a short 2 aa intracellular cytoplasmic domain.

MOLECULAR MASS

POST-TRANSCRIPTIONAL MODIFICATION

Alternative splicing yields 2 different isoforms.  The isoforms have been decribed but their full length has not been determined.

POST-TRANSLATIONAL MODIFICATION

CLEC5A has a glycosylation site.

Ligands
LIGANDS AND MOLECULES ASSOCIATED WITH CLEC5A: No information.

Function
Members of this lectin-like family share a common protein fold and have diverse functions such as cell adhesion, cell-cell signaling, glycoprotein turnover and roles in inflammation and immune response.  CLCE5A interacts with Dap12 and may play a role in cell activation.  CLEC5A may be involved in proinflammatory activation of myeloid cells by tyrosine kinase-binding protein (TYROBP)-mediating signaling in a calcium-dependent manner.

BIOCHEMICAL ACTIVITY: No information.

DISEASE RELEVANCE AND FUNCTION OF CLEC5A IN INTACT ANIMAL: No information.

Comments
MOLECULAR INTERACTION-
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CLEC5A: No information.

SUBSTRATES: No information.

ENZYMES WHICH MODIFY CLEC5A: No information.

Database accession numbers
AnimalPIRSWISSPROTEMGBL/GENBANK
 
HumanEntrezgene23601Q9NY25
Antibodies

Revised June 25, 2008


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