{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["di Cicco G"],"pubmed_abstract":["Budding yeast Rad9, like its orthologs, controls two aspects of the cellular response to DNA double strand breaks (DSBs) - signalling of the DNA damage checkpoint and DNA end resection. Rad9 binds to damaged chromatin via modified nucleosomes independently of the cell cycle phase. Additionally, Rad9 engages in a cell cycle-regulated interaction with Dpb11 and the 9-1-1 clamp, generating a second pathway that recruits Rad9 to DNA damage sites. Binding to Dpb11 depends on specific S/TP phosphorylation sites of Rad9, which are modified by cyclin-dependent kinase (CDK). Here, we show that these sites additionally become phosphorylated upon DNA damage. We define the requirements for DNA damage-induced S/TP phosphorylation of Rad9 and show that it is independent of the cell cycle or CDK activity"],"journal":["Scientific reports"],"pagination":["11650"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5599684"],"repository":["biostudies-literature"],"pubmed_title":["A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage."],"pmcid":["PMC5599684"],"pubmed_authors":["di Cicco G","Bantele SCS","Reusswig KU","Pfander B"],"additional_accession":[]},"is_claimable":false,"name":"A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage.","description":"Budding yeast Rad9, like its orthologs, controls two aspects of the cellular response to DNA double strand breaks (DSBs) - signalling of the DNA damage checkpoint and DNA end resection. Rad9 binds to damaged chromatin via modified nucleosomes independently of the cell cycle phase. Additionally, Rad9 engages in a cell cycle-regulated interaction with Dpb11 and the 9-1-1 clamp, generating a second pathway that recruits Rad9 to DNA damage sites. Binding to Dpb11 depends on specific S/TP phosphorylation sites of Rad9, which are modified by cyclin-dependent kinase (CDK). Here, we show that these sites additionally become phosphorylated upon DNA damage. We define the requirements for DNA damage-induced S/TP phosphorylation of Rad9 and show that it is independent of the cell cycle or CDK activity","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2025-04-05T14:17:45.441Z","creation":"2019-03-27T02:56:27Z"},"accession":"S-EPMC5599684","cross_references":{"pubmed":["28912563"],"doi":["10.1038/s41598-017-11937-z"]}}