CD163 — CD163 molecule
CD163 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.
CD163's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Monocytes | Tissue-Resident Macrophage Lysosomal & pahgocytosis | AP2A2, BLVRB, FAH, FCGRT, HTRA1, MKKS, MYO7A, RNASE1 +6 more | View in SCUBA |
About the gene
| Synonyms | M130, MM130, SCARI1 |
|---|---|
| Chromosome | 12: 7470811-7503893 |
| Predicted location | Intracellular, Membrane, Secreted |
| Essential gene | No |
| Protein class | CD markers, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins, Predicted secreted proteins |
| Biological process | Acute phase, Inflammatory response |
Function
Acute phase-regulated receptor involved in clearance and endocytosis of hemoglobin/haptoglobin complexes by macrophages and may thereby protect tissues from free hemoglobin-mediated oxidative damage. May play a role in the uptake and recycling of iron, via endocytosis of hemoglobin/haptoglobin and subsequent breakdown of heme. Binds hemoglobin/haptoglobin complexes in a calcium-dependent and pH- dependent manner. Exhibits a higher affinity for complexes of hemoglobin and multimeric haptoglobin of HP*1F phenotype than for complexes of hemoglobin and dimeric haptoglobin of HP*1S phenotype. Induces a cascade of intracellular signals that involves tyrosine kinase-dependent calcium mobilization, inositol triphosphate production and secretion of IL6 and CSF1. Isoform 3 exhibits the higher capacity for ligand endocytosis and the more pronounced surface expression when expressed in cells. After shedding, the soluble form (sCD163) may play an anti- inflammatory role, and may be a valuable diagnostic parameter for monitoring macrophage activation in inflammatory conditions
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.