CLEC4D — C-type lectin domain family 4 member D
CLEC4D belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
CLEC4D's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Neutrophils | Specific Granule Release Degranulation | BMX, CA4, CKAP4, GPAT3, KBTBD7, MMP9, VIM |
About the gene
| Synonyms | CD368, CLECSF8, Dectin-3, MCL, Mpcl |
|---|---|
| Chromosome | 12: 8509475-8522366 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | CD markers, Predicted intracellular proteins |
| Biological process | Adaptive immunity, Immunity, Innate immunity |
Function
Calcium-dependent lectin that acts as a pattern recognition receptor (PRR) of the innate immune system: recognizes damage- associated molecular patterns (DAMPs) of pathogen-associated molecular patterns (PAMPs) of bacteria and fungi. The PAMPs include alpha-mannans on C.albicans hypheas and mycobacterial trehalose 6,6'-dimycolate (TDM). Interacts with signaling adapter Fc receptor gamma chain/FCER1G, likely via CLEC4E, to form a functional complex in myeloid cells (By similarity). Binding of mycobacterial TDM or C.albicans alpha-mannans to this receptor complex leads to phosphorylation of the immunoreceptor tyrosine-based activation motif (ITAM) of FCER1G, triggering activation of SYK, CARD9 and NF-kappa-B, consequently driving maturation of antigen-presenting cells and shaping antigen-specific priming of T-cells toward effector T-helper 1 and T- helper 17 cell subtypes. The heterodimer formed with CLEC6A is active against fungal infection. Functions as an endocytic receptor. May be involved in antigen uptake at the site of infection, either for clearance of the antigen, or for processing and further presentation to T-cells.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.