CHFR — Checkpoint with forkhead and ring finger domains
CHFR 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.
CHFR's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Macrophages | Endolysosomal Trafficking Vesicular traficking | ANKRD10, ATP1A1, ATP6V0A1, CHML, FAR1, FBXL5, GSAP, HAPSTR1 +21 more | View in SCUBA |
About the gene
| Synonyms | FLJ10796, RNF196 |
|---|---|
| Chromosome | 12: 132822187-132956304 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Cancer-related genes, Enzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins |
| Molecular function | Transferase |
| Biological process | Cell cycle, Cell division, Mitosis, Ubl conjugation pathway |
Function
E3 ubiquitin-protein ligase that functions in the antephase checkpoint by actively delaying passage into mitosis in response to microtubule poisons. Acts in early prophase before chromosome condensation, when the centrosome move apart from each other along the periphery of the nucleus. Probably involved in signaling the presence of mitotic stress caused by microtubule poisons by mediating the 'Lys- 48'-linked ubiquitination of target proteins, leading to their degradation by the proteasome. Promotes the ubiquitination and subsequent degradation of AURKA and PLK1. Probably acts as a tumor suppressor, possibly by mediating the polyubiquitination of HDAC1, leading to its degradation. May also promote the formation of 'Lys-63'- linked polyubiquitin chains and functions with the specific ubiquitin- conjugating UBC13-MMS2 (UBE2N-UBE2V2) heterodimer. Substrates that are polyubiquitinated at 'Lys-63' are usually not targeted for degradation, but are rather involved in signaling cellular stress.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.