{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["27(7)"],"submitter":["Niida H"],"pubmed_abstract":["Chk1 is a multifunctional protein kinase that plays essential roles in cell survival and cell cycle checkpoints. Chk1 is phosphorylated at multiple sites by several protein kinases, but the precise effects of these phosphorylations are largely unknown. Using a knockout-knockin system, we examined the abilities of Chk1 mutants to reverse the defects of Chk1-null cells. Wild-type Chk1 could rescue all the defects of Chk1-null cells. Like endogenous Chk1, wild-type Chk1 localized in both the cytoplasm and the nucleus, and its centrosomal association was enhanced by DNA damage. The mutation at S345 resulted in mitotic catastrophe, impaired checkpoints, and loss of the ability to localize in the cytoplasm, but the mutant retained the ability to be released from chromatin upon encountering genot"],"journal":["Molecular and cellular biology"],"pagination":["2572-81"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1899884"],"repository":["biostudies-literature"],"pubmed_title":["Specific role of Chk1 phosphorylations in cell survival and checkpoint activation."],"pmcid":["PMC1899884"],"pubmed_authors":["Banerjee B","Nakanishi M","Hande MP","Katsuno Y","Niida H"],"additional_accession":[]},"is_claimable":false,"name":"Specific role of Chk1 phosphorylations in cell survival and checkpoint activation.","description":"Chk1 is a multifunctional protein kinase that plays essential roles in cell survival and cell cycle checkpoints. Chk1 is phosphorylated at multiple sites by several protein kinases, but the precise effects of these phosphorylations are largely unknown. Using a knockout-knockin system, we examined the abilities of Chk1 mutants to reverse the defects of Chk1-null cells. Wild-type Chk1 could rescue all the defects of Chk1-null cells. Like endogenous Chk1, wild-type Chk1 localized in both the cytoplasm and the nucleus, and its centrosomal association was enhanced by DNA damage. The mutation at S345 resulted in mitotic catastrophe, impaired checkpoints, and loss of the ability to localize in the cytoplasm, but the mutant retained the ability to be released from chromatin upon encountering genot","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Apr","modification":"2025-04-19T13:07:40.077Z","creation":"2019-03-27T02:04:14Z"},"accession":"S-EPMC1899884","cross_references":{"pubmed":["17242188"],"doi":["10.1128/MCB.01611-06","10.1128/mcb.01611-06"]}}