a cell-cycle regulatory protein that Interacts with cyclin-CDK2 and -CDK4, inhibiting cell cycle progression at G1. Its expression is tightly controlled by p53, through which this protein mediates the p53-dependent cell cycle arrest at G1 phase. Note: This description may include information from UniProtKB.
Protein type: Cell cycle regulation; Inhibitor protein
Cellular Component: nucleoplasm; cyclin-dependent protein kinase holoenzyme complex; nucleus; cytosol
Molecular Function: cyclin-dependent protein kinase inhibitor activity; protein binding; cyclin binding; cyclin-dependent protein kinase activating kinase activity; metal ion binding; protein complex binding
Biological Process: nerve growth factor receptor signaling pathway; response to toxin; response to arsenic; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; negative regulation of cell proliferation; positive regulation of fibroblast proliferation; positive regulation of B cell proliferation; cell cycle arrest; G2/M transition of mitotic cell cycle; response to UV; response to corticosterone stimulus; response to drug; epidermal growth factor receptor signaling pathway; organ regeneration; fibroblast growth factor receptor signaling pathway; phosphoinositide-mediated signaling; negative regulation of cyclin-dependent protein kinase activity; response to organic nitrogen; positive regulation of programmed cell death; response to hyperoxia; Ras protein signal transduction; cellular response to extracellular stimulus; innate immune response; regulation of protein import into nucleus, translocation; negative regulation of phosphorylation; regulation of cyclin-dependent protein kinase activity; mitotic cell cycle; negative regulation of cell growth; response to DNA damage stimulus; G1/S transition of mitotic cell cycle; negative regulation of apoptosis
SS: 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.