a protein kinase of the CAMKL family. Required for checkpoint mediated cell cycle arrest in response to DNA damage or the presence of unreplicated DNA. May also negatively regulate cell cycle progression during unperturbed cell cycles. Plays an important role in both S and G2 checkpoints, embryonic development and tumor suppression. Phosphorylated and activated by ATM/ATR following DNA damage, it binds to single-stranded DNA and DNA ends and has a role in the repair of double strand breaks. Activated Chk1 can phosphorylate and inactivate cdc25C via phosphorylation and 14-3-3 binding, blocking the activation of cdc2 and transition into M-phase. Other substrates include p53. Implicated in resistance to apoptosis in response to chemotherapy. Inhibitors under development to chemosensitize tumors. Somatic mutations found in stomach tumors, and in colon and endometrial tumors, where CHK1 may be a target of microsatellite instability. Inhibitors: SB218078, UNC-01. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Protein kinase, CAMK; EC 188.8.131.52; Protein kinase, Ser/Thr (non-receptor); CAMK group; CAMKL family; CHK1 subfamily
Molecular Function: protein serine/threonine kinase activity; identical protein binding; protein binding; ATP binding
Biological Process: DNA damage induced protein phosphorylation; regulation of mitotic centrosome separation; regulation of S phase; peptidyl-threonine phosphorylation; DNA repair; regulation of cell proliferation; chromatin-mediated maintenance of transcription; negative regulation of mitosis; DNA damage checkpoint; G2/M transition of mitotic cell cycle; G2/M transition DNA damage checkpoint; DNA replication; response to DNA damage stimulus
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.