CDK6
Gene Ontology Biological Process
- G1/S transition of mitotic cell cycle [TAS]
- astrocyte development [ISS]
- cell cycle arrest [TAS]
- cell dedifferentiation [IMP]
- dentate gyrus development [ISS]
- generation of neurons [ISS]
- gliogenesis [IMP]
- lateral ventricle development [ISS]
- mitotic cell cycle [TAS]
- negative regulation of cell cycle [IDA]
- negative regulation of cell differentiation [TAS]
- negative regulation of cell proliferation [TAS]
- negative regulation of cellular senescence [IDA]
- negative regulation of epithelial cell proliferation [IMP]
- negative regulation of myeloid cell differentiation [IDA]
- negative regulation of osteoblast differentiation [IDA]
- positive regulation of cell-matrix adhesion [IDA]
- positive regulation of fibroblast proliferation [IMP]
- protein phosphorylation [IDA]
- regulation of cell motility [ISS]
- regulation of erythrocyte differentiation [IMP]
- regulation of gene expression [IDA, IMP]
- response to virus [IEP]
- type B pancreatic cell development [IDA]
Gene Ontology Molecular Function
TJP2
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Phosphorylation)
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
A systematic screen for CDK4/6 substrates links FOXM1 phosphorylation to senescence suppression in cancer cells.
Cyclin D-dependent kinases (CDK4 and CDK6) are positive regulators of cell cycle entry and they are overactive in the majority of human cancers. However, it is currently not completely understood by which cellular mechanisms CDK4/6 promote tumorigenesis, largely due to the limited number of identified substrates. Here we performed a systematic screen for substrates of cyclin D1-CDK4 and cyclin D3-CDK6. ... [more]
Throughput
- High Throughput
Curated By
- BioGRID