UBQLN2 — Ubiquilin 2
UBQLN2 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.
UBQLN2's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Gamma-delta T cells | Osmotic Stress Response Stress | BAZ1A, BMPR2, HIPK3, HTT, LIX1L, MAPRE2, NFAT5, RALGAPB +6 more |
About the gene
| Synonyms | Chap1, CHAP1/DSK2, Dsk2, LIC-2, N4BP4, PLIC-2, PLIC2, RIHFB2157 |
|---|---|
| Chromosome | X: 56563627-56567868 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins |
| Biological process | Autophagy |
Function
Plays an important role in the regulation of different protein degradation mechanisms and pathways including ubiquitin- proteasome system (UPS), autophagy and the endoplasmic reticulum- associated protein degradation (ERAD) pathway. Mediates the proteasomal targeting of misfolded or accumulated proteins for degradation by binding (via UBA domain) to their polyubiquitin chains and by interacting (via ubiquitin-like domain) with the subunits of the proteasome. Plays a role in the ERAD pathway via its interaction with ER-localized proteins FAF2/UBXD8 and HERPUD1 and may form a link between the polyubiquitinated ERAD substrates and the proteasome. Involved in the regulation of macroautophagy and autophagosome formation; required for maturation of autophagy-related protein LC3 from the cytosolic form LC3-I to the membrane-bound form LC3-II and may assist in the maturation of autophagosomes to autolysosomes by mediating autophagosome-lysosome fusion. Negatively regulates the endocytosis of GPCR receptors: AVPR2 and ADRB2, by specifically reducing the rate at which receptor-arrestin complexes concentrate in clathrin-coated pits (CCPs).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.