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: Cell cycle regulation; Protein kinase, CMGC; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 22.214.171.124; CMGC group; CDK family; CDK4 subfamily; CDK/CDK4 subfamily
Cellular Component: chromatin; cyclin-dependent protein kinase holoenzyme complex; cytosol; nuclear membrane; nucleolus; nucleoplasm; nucleus; perinuclear region of cytoplasm; tight junction; transcription factor complex
Molecular Function: ATP binding; cyclin binding; cyclin-dependent protein kinase activity; cyclin-dependent protein kinase regulator activity; protein binding; protein complex binding
Biological Process: cell division; circadian rhythm; establishment and/or maintenance of chromatin architecture; G1/S transition of mitotic cell cycle; lens development in camera-type eye; mitotic cell cycle; organ regeneration; positive regulation of apoptosis; positive regulation of cell proliferation; positive regulation of cell size; positive regulation of fibroblast proliferation; positive regulation of translation; protein amino acid phosphorylation; regulation of gene expression; regulation of protein kinase activity; response to drug; response to hyperoxia; response to lead ion; response to testosterone stimulus; response to toxin; signal transduction
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.