TRIM3
Gene Ontology Biological Process
Gene Ontology Molecular Function
CDKN1A
Gene Ontology Biological Process
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [IDA, TAS]
- Fc-epsilon receptor signaling pathway [TAS]
- G1/S transition of mitotic cell cycle [IDA, TAS]
- G2/M transition of mitotic cell cycle [IMP]
- Ras protein signal transduction [IEP]
- cell cycle arrest [IDA, IMP]
- cellular response to DNA damage stimulus [IMP]
- cellular response to extracellular stimulus [IMP]
- cellular response to ionizing radiation [IMP]
- cellular senescence [IMP]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- intrinsic apoptotic signaling pathway [TAS]
- mitotic cell cycle [TAS]
- negative regulation of G1/S transition of mitotic cell cycle [IGI]
- negative regulation of cell growth [IDA]
- negative regulation of cell proliferation [IDA, IMP]
- negative regulation of phosphorylation [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- phosphatidylinositol-mediated signaling [TAS]
- positive regulation of fibroblast proliferation [IMP]
- positive regulation of protein kinase activity [IDA]
- positive regulation of reactive oxygen species metabolic process [IMP]
- protein phosphorylation [IDA]
- regulation of cyclin-dependent protein serine/threonine kinase activity [TAS]
- stress-induced premature senescence [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Ubiquitination)
An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation.
Publication
The ability of TRIM3 to induce growth arrest depends on RING-dependent E3 ligase activity.
Mutation of the TRIM (tripartite motif)-NHL family members brat and mei-P26 perturb the differentiation of transit-amplifying progenitor cells resulting in tumour-like phenotypes. The NHL (named after the NCL1, HT2A and LIN41 repeat) domain is essential for their growth suppressive activity, and they can induce cell-cycle exit in a RING-independent manner. TRIM3 is the only bona fide tumour suppressor in the ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID