ADGRF5 — Adhesion G protein-coupled receptor F5
ADGRF5 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.
ADGRF5's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Endothelial | Endothelial Junction Identity Endothelial cell development | AKAP13, CDH5, CXCL12, DENND5A, FGF12, FURIN, HSPA12B, NES +13 more | View in SCUBA |
| Fibroblasts | ICC niche interactaion Gut motility | ABCC9, ANO1, CD36, CFHR1, ESAM, FHL5, HOPX, HRH2 +10 more | View in SCUBA |
| Lymphatic endothelial | Endothelial Receptor Signaling endothelial development | ART4, ENTREP1, FLRT2, P3H2, PDGFC, PLSCR4, SNCAIP, SRGAP3 +2 more | View in SCUBA |
About the gene
| Synonyms | DKFZp564O1923, GPR116, KIAA0758 |
|---|---|
| Chromosome | 6: 46852522-46954943 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | G-protein coupled receptors, Plasma proteins, Predicted membrane proteins |
| Molecular function | G-protein coupled receptor, Receptor, Transducer |
Function
Adhesion G protein-coupled receptor. In alveolar type II (ATII or AT2) cells, required for normal lung surfactant homeostasis. Modulation of both surfactant secretion and uptake by ATII cells is mediated by the downstream activation of GNAQ/GNA11 proteins and may be a consequence of increased cortical F-actin assembly induced by ADGRF5 activation. In the kidney, may play a role in the regulation of acid excretion into the primary urine, possibly by regulating the surface expression of V-ATPase proton pump (By similarity). As a receptor for soluble FNDC4 (sFNDC4), required for proper systemic glucose tolerance, specifically sensitizing white adipose tissue to insulin. Also plays a role in sFNDC4-induced decrease of local inflammation in white adipose tissue.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.