RNF144B — Ring finger protein 144B
RNF144B 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.
RNF144B's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Macrophages | Innate Immune Dampening Innate immunity | DCAF6, ELL2, FGD4, FKBP5, IRAK3, MAP2K4, MOB3B, PACSIN2 +10 more | View in SCUBA |
| Monocytes | Inflammatory Monocyte Activation Inflammatory | ALDOA, C11orf98, CLEC2B, CNIH4, CRIP1, GRINA, IFITM2, LEPROTL1 +5 more | View in SCUBA |
About the gene
| Synonyms | bA528A10.3, IBRDC2, P53RFP |
|---|---|
| Chromosome | 6: 18387350-18468870 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | Enzymes, Metabolic proteins, Predicted membrane proteins |
| Molecular function | Transferase |
| Biological process | Apoptosis, Ubl conjugation pathway |
Function
E3 ubiquitin-protein ligase which accepts ubiquitin from E2 ubiquitin-conjugating enzymes UBE2L3 and UBE2L6 in the form of a thioester and then directly transfers the ubiquitin to targeted substrates such as LCMT2, thereby promoting their degradation. Induces apoptosis via a p53/TP53-dependent but caspase-independent mechanism. Plays a crucial role in maintaining the genomic stability by controlling the degradation of multiple proteins involved in mitotic progression and DNA damage. Regulates epithelial homeostasis by mediating degradation of CDKN1A and isoform 2 of TP63. Plays a regulatory role in innate immunity by negatively regulating IRF3 activation and IFN-beta production. Mechanistically, inhibits TBK1 phosphorylation and 'Lys-63'-linked polyubiquitination independently of its E3 ligase activity. Alternatively, promotes 'Lys-27' and 'Lys-33'-linked ubiquitination of IFIH1/MDA5, promoting selective autophagic degradation of IFIH1/MDA5 to inhibit antiviral response.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.