SORCS2 — Sortilin related VPS10 domain containing receptor 2
SORCS2 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.
SORCS2's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Fibroblasts | Heparan Sulfate Remodeling ECM remodeling | ALDH1A3, COL12A1, FAM171B, FANCC, FHOD3, GREB1, HS6ST1, JMJD1C +11 more | View in SCUBA |
About the gene
| Synonyms | KIAA1329 |
|---|---|
| Chromosome | 4: 7192538-7742836 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | Plasma proteins, Predicted membrane proteins |
Function
The heterodimer formed by NGFR and SORCS2 functions as receptor for the precursor forms of NGF (proNGF) and BDNF (proBDNF). ProNGF and proBDNF binding both promote axon growth cone collapse (in vitro). Plays a role in the regulation of dendritic spine density in hippocampus neurons (By similarity). Required for normal neurite branching and extension in response to BDNF. Plays a role in BDNF-dependent hippocampal synaptic plasticity. Together with NGFR and NTRK2, is required both for BDNF-mediated synaptic long-term depression and long-term potentiation. ProNGF binding promotes dissociation of TRIO from the heterodimer, which leads to inactivation of RAC1 and/or RAC2 and subsequent reorganization of the actin cytoskeleton. Together with the retromer complex subunit VPS35, required for normal expression of GRIN2A at synapses and dendritic cell membranes. Required for normal expression of the amino acid transporter SLC1A1 at the cell membrane, and thereby contributes to protect cells against oxidative stress (By similarity). Does not promote Schwann cell apoptosis in response to proBDNF. SorCS2 104 kDa chain and SorCS2 18 kDa chain together promote Schwann cell apoptosis in response to proBDNF
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.