RUBCN — Rubicon autophagy regulator
RUBCN belongs to a gene co-expression module in 2 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.
RUBCN's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | AKT survival signaling TCR/AP1/NFKb pathway | ABHD2, AKT1, ARL14EP, ATF7, ATP6AP1, CHD8, GNGT2, IP6K2 +10 more | View in SCUBA |
| Gamma-delta T cells | NK-like Mature gd-T cytotoxicity | ABHD2, ATG9A, CEP78, HAVCR2, HSH2D, IFIT2, ITGAX, KIR2DL1 +14 more |
About the gene
| Synonyms | KIAA0226, rubicon, rundataxin |
|---|---|
| Chromosome | 3: 197668867-197749727 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Disease related genes, Human disease related genes, Predicted intracellular proteins |
| Biological process | Autophagy, Endocytosis, Immunity, Phagocytosis |
Function
Inhibits PIK3C3 activity; under basal conditions negatively regulates PI3K complex II (PI3KC3-C2) function in autophagy. Negatively regulates endosome maturation and degradative endocytic trafficking and impairs autophagosome maturation process. Can sequester UVRAG from association with a class C Vps complex (possibly the HOPS complex) and negatively regulates Rab7 activation. Involved in regulation of pathogen-specific host defense of activated macrophages. Following bacterial infection promotes NADH oxidase activity by association with CYBA thereby affecting TLR2 signaling and probably other TLR-NOX pathways. Stabilizes the CYBA:CYBB NADPH oxidase heterodimer, increases its association with TLR2 and its phagosome trafficking to induce antimicrobial burst of ROS and production of inflammatory cytokines. Following fungal or viral infection (implicating CLEC7A (dectin-1)-mediated myeloid cell activation or RIGI-dependent sensing of RNA viruses) negatively regulates pro-inflammatory cytokine production by association with CARD9 and sequestering it from signaling complexes.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.