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: CAMK group; CAMKL family; CHK1 subfamily; EC 22.214.171.124; Kinase, protein; Protein kinase, CAMK; Protein kinase, Ser/Thr (non-receptor); Tumor suppressor
Molecular Function: kinase activity; protein binding; protein domain specific binding; protein kinase activity; protein serine/threonine kinase activity
Biological Process: chromatin-mediated maintenance of transcription; DNA damage checkpoint; DNA damage induced protein phosphorylation; DNA repair; DNA replication; G2/M transition DNA damage checkpoint; negative regulation of mitosis; peptidyl-threonine phosphorylation; positive regulation of cell cycle; regulation of mitotic centrosome separation; response to DNA damage stimulus