RNF20 — Ring finger protein 20
RNF20 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.
RNF20's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Gamma-delta T cells | Interferon Stimulated Genes Inflammation | AATF, ACSL5, ACTR10, AGL, DDX60, DTX3L, HCLS1, HIF1AN +14 more |
About the gene
| Synonyms | BRE1, BRE1A, FLJ11189, FLJ20382, hBRE1, KAIA2779 |
|---|---|
| Chromosome | 9: 101533853-101563344 |
| Predicted location | Intracellular |
| Essential gene | Yes |
| Protein class | Enzymes, Essential proteins, Metabolic proteins, Predicted intracellular proteins |
| Molecular function | Chromatin regulator, Transferase |
| Biological process | Host-virus interaction, Ubl conjugation pathway |
Function
Component of the RNF20/40 E3 ubiquitin-protein ligase complex that mediates monoubiquitination of 'Lys-120' of histone H2B (H2BK120ub1). H2BK120ub1 gives a specific tag for epigenetic transcriptional activation and is also prerequisite for histone H3 'Lys-4' and 'Lys-79' methylation (H3K4me and H3K79me, respectively). It thereby plays a central role inb histone code and gene regulation. The RNF20/40 complex forms a H2B ubiquitin ligase complex in cooperation with the E2 enzyme UBE2A or UBE2B; reports about the cooperation with UBE2E1/UBCH are contradictory. Required for transcriptional activation of Hox genes. Recruited to the MDM2 promoter, probably by being recruited by p53/TP53, and thereby acts as a transcriptional coactivator. Mediates the polyubiquitination of isoform 2 of PA2G4 in cancer cells leading to its proteasome-mediated degradation. (Microbial infection) Promotes the human herpesvirus 8 (KSHV) lytic cycle by inducing the expression of lytic viral genes including the latency switch gene RTA/ORF50
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.