a protein kinase of the CDK family that is important for cell cycle G1 phase progression. Its activity is restricted to the G1-S phase. Controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). Phosphorylates the retinoblastoma gene product (Rb). Point mutations found in somatic and familial melanoma. Amplified in sarcomas, glioma and lymphoma. Amplified, methylated or deleted in head and neck squamous cell carcinoma. Overexpression drives epithelial tumors in mice. Disruption makes mice resistant to cancer. Inhibitor: PD332991. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, CMGC; Kinase, protein; Cell cycle regulation; Protein kinase, Ser/Thr (non-receptor); EC 22.214.171.124; CMGC group; CDK family; CDK/CDK4 subfamily; CDK4 subfamily
Cellular Component: nucleoplasm; transcription factor complex; nuclear membrane; tight junction; perinuclear region of cytoplasm; nucleolus; cyclin-dependent protein kinase holoenzyme complex; chromatin; nucleus; cytosol
Molecular Function: cyclin binding; protein binding; cyclin-dependent protein kinase activity; protein complex binding; cyclin-dependent protein kinase regulator activity; ATP binding
Biological Process: lens development in camera-type eye; response to drug; circadian rhythm; establishment and/or maintenance of chromatin architecture; organ regeneration; positive regulation of cell size; positive regulation of translation; positive regulation of apoptosis; response to toxin; response to testosterone stimulus; signal transduction; protein amino acid phosphorylation; positive regulation of fibroblast proliferation; response to hyperoxia; regulation of gene expression; cell division; response to lead ion; positive regulation of cell proliferation; mitotic cell cycle; regulation of protein kinase activity; G1/S transition of mitotic cell cycle
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.