KIR2DL4 — Killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4
KIR2DL4 belongs to a gene co-expression module in 3 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.
KIR2DL4's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD8⁺ T cells | Tissue residence Gut residence | AFAP1L2, FAM3C, HTRA1, KRT81, KRT86, NBL1, PLPP1, PTPN6 +1 more | View in SCUBA |
| Gamma-delta T cells | NK Receptor Expression cytotoxicity | CRACR2B, GFOD1, GPR171, GPR55, GSTM4, KLRC2, KLRC3, MORF4L2 +4 more | |
| Natural Killer cells | NK Checkpoint Receptors Immune regulation | CD7, CD96, CRACR2B, DAPK2, ECH1, ECI2, ISYNA1, MAP4 +5 more | View in SCUBA |
About the gene
| Synonyms | 103AS, 15.212, CD158D |
|---|---|
| Chromosome | 19: 54803610-54814517 |
| Predicted location | Intracellular, Membrane |
| Essential gene | No |
| Protein class | CD markers, Predicted intracellular proteins, Predicted membrane proteins |
| Molecular function | Receptor |
Function
Receptor for non-classical major histocompatibility class Ib HLA-G molecules. Recognizes HLA-G in complex with B2M/beta-2 microglobulin and a nonamer self-peptide (peptide-bound HLA-G-B2M). In decidual NK cells, binds peptide-bound HLA-G-B2M complex and triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy. May play a role in balancing tolerance and antiviral-immunity at maternal-fetal interface by keeping in check the effector functions of NK, CD8+ T cells and B cells. Upon interaction with peptide-bound HLA-G-B2M, initiates signaling from the endosomal compartment leading to downstream activation of PRKDC-XRCC5 and AKT1, and ultimately triggering NF-kappa-B-dependent pro-inflammatory response.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.