CD93 — CD93 molecule
CD93 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.
CD93's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Endothelial | Endothelial Angiogenic Identity Endothelial cell development | ACTN4, ADGRL4, APBB2, CAVIN1, CLEC14A, CLIC4, ESAM, MYH9 +5 more | View in SCUBA |
About the gene
| Synonyms | C1qR(P), C1QR1, C1qRP, CDw93, dJ737E23.1, ECSM3, MXRA4 |
|---|---|
| Chromosome | 20: 23079360-23086324 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | CD markers, Plasma proteins, Predicted membrane proteins |
| Molecular function | Receptor |
| Biological process | Cell adhesion, Host-virus interaction |
Function
Cell surface receptor that plays a role in various physiological processes including inflammation, phagocytosis, and cell adhesion. Plays a role in phagocytosis and enhances the uptake of apoptotic cells and immune complexes by acting as a receptor for defense collagens including surfactant protein A/SFTPA1, C1q, and mannose-binding lectin (MBL2). Plays a role in the regulation of endothelial cell function and adhesion by activating angiogenesis. Mechanistically, exerts its angiogenic function by associating with beta-dystroglycan, leading to SRC- dependent phosphorylation and subsequent recruitment of CBL. In turn, CBL provides a docking site for downstream signaling components, such as CRKL to enhance cell migration. Participates in angiogenesis also by acting as a receptor for the ECM pan-endothelial glycoprotein multimerin-2/MMRN2 and IGFBP7 ligands. Both ligands play a non-redundant role in CD93-mediated endothelial cell function. Acts as a key regulator of endothelial barrier function through modulating VEGFR2 function (By similarity).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.