Serine/threonine-protein kinase involved in the control of the cell cycle; essential for meiosis, but dispensable for mitosis. Phosphorylates CTNNB1, USP37, p53/TP53, NPM1, CDK7, RB1, BRCA2, MYC, NPAT, EZH2. Triggers duplication of centrosomes and DNA. Acts at the G1-S transition to promote the E2F transcriptional program and the initiation of DNA synthesis, and modulates G2 progression; controls the timing of entry into mitosis/meiosis by controlling the subsequent activation of cyclin B/CDK1 by phosphorylation, and coordinates the activation of cyclin B/CDK1 at the centrosome and in the nucleus. Crucial role in orchestrating a fine balance between cellular proliferation, cell death, and DNA repair in human embryonic stem cells (hESCs). Activity of CDK2 is maximal during S phase and G2; activated by interaction with cyclin E during the early stages of DNA synthesis to permit G1-S transition, and subsequently activated by cyclin A2 (cyclin A1 in germ cells) during the late stages of DNA replication to drive the transition from S phase to mitosis, the G2 phase. EZH2 phosphorylation promotes H3K27me3 maintenance and epigenetic gene silencing. Phosphorylates CABLES1. Cyclin E/CDK2 prevents oxidative stress-mediated Ras-induced senescence by phosphorylating MYC. Involved in G1-S phase DNA damage checkpoint that prevents cells with damaged DNA from initiating mitosis; regulates homologous recombination-dependent repair by phosphorylating BRCA2, this phosphorylation is low in S phase when recombination is active, but increases as cells progress towards mitosis. In response to DNA damage, double-strand break repair by homologous recombination a reduction of CDK2-mediated BRCA2 phosphorylation. Phosphorylation of RB1 disturbs its interaction with E2F1. NPM1 phosphorylation by cyclin E/CDK2 promotes its dissociates from unduplicated centrosomes, thus initiating centrosome duplication. Cyclin E/CDK2-mediated phosphorylation of NPAT at G1-S transition and until prophase stimulates the NPAT-mediated activation of histone gene transcription during S phase. Required for vitamin D-mediated growth inhibition by being itself inactivated. Involved in the nitric oxide- (NO) mediated signaling in a nitrosylation/activation-dependent manner. USP37 is activated by phosphorylation and thus triggers G1-S transition. CTNNB1 phosphorylation regulates insulin internalization. Phosphorylates FOXP3 and negatively regulates its transcriptional activity and protein stability. Phosphorylates CDK2AP2. Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily. 2 alternatively spliced human isoforms have been reported. Note: This description may include information from UniProtKB.
Protein type: CDK family; CDK/CDK1 subfamily; CDK1 subfamily; CMGC group; Cell cycle regulation; EC 22.214.171.124; Kinase, protein; Protein kinase, CMGC; Protein kinase, Ser/Thr (non-receptor)
Molecular Function: ATP binding; cyclin binding; cyclin-dependent protein kinase activity; cyclin-dependent protein serine/threonine kinase activity; magnesium ion binding; protein binding; protein domain specific binding; protein serine/threonine kinase activity
Biological Process: anaphase-promoting complex-dependent catabolic process; cell division; cellular response to nitric oxide; centriole replication; centrosome duplication; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; DNA repair; DNA replication; G1/S transition of mitotic cell cycle; G2/M transition of mitotic cell cycle; histone phosphorylation; meiotic cell cycle; mitotic G1 DNA damage checkpoint; negative regulation of transcription by RNA polymerase II; peptidyl-serine phosphorylation; positive regulation of cell proliferation; positive regulation of DNA-dependent DNA replication initiation; positive regulation of transcription, DNA-templated; potassium ion transport; protein phosphorylation; Ras protein signal transduction; regulation of gene silencing; regulation of signal transduction by p53 class mediator