{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(23)"],"submitter":["Rimmele P"],"pubmed_abstract":["Oncogenes trigger replicative stress that can lead to genetic instability, which participates in cancer progression. Thus, determining how cells cope with replicative stress can help our understanding of oncogenesis and lead to the identification of new antitumor treatment targets. We previously showed that constitutive overexpression of the oncogenic transcription factor Spi1/PU.1 leads to pre-leukemic cells that have a shortened S phase duration with an increased replication fork speed and increased mutability in the absence of DNA breaks. Here, we demonstrate that the S phase checkpoint protein CHK1 is maintained in a low phosphorylation state in Spi1/PU.1-overexpressing cells and provide evidence that this is not due to negative control of its primary kinase ATR. Notably, we found that"],"journal":["Oncotarget"],"pagination":["37104-37114"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5514894"],"repository":["biostudies-literature"],"pubmed_title":["The Spi1/PU.1 transcription factor accelerates replication fork progression by increasing PP1 phosphatase in leukemia."],"pmcid":["PMC5514894"],"pubmed_authors":["Delestre L","Rosselli F","Ridinger-Saison M","Rimmele P","Esposito M","Guillouf C","Guervilly JH","Despras E","Moreau-Gachelin F"],"additional_accession":[]},"is_claimable":false,"name":"The Spi1/PU.1 transcription factor accelerates replication fork progression by increasing PP1 phosphatase in leukemia.","description":"Oncogenes trigger replicative stress that can lead to genetic instability, which participates in cancer progression. Thus, determining how cells cope with replicative stress can help our understanding of oncogenesis and lead to the identification of new antitumor treatment targets. We previously showed that constitutive overexpression of the oncogenic transcription factor Spi1/PU.1 leads to pre-leukemic cells that have a shortened S phase duration with an increased replication fork speed and increased mutability in the absence of DNA breaks. Here, we demonstrate that the S phase checkpoint protein CHK1 is maintained in a low phosphorylation state in Spi1/PU.1-overexpressing cells and provide evidence that this is not due to negative control of its primary kinase ATR. Notably, we found that","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jun","modification":"2025-04-22T17:46:13.071Z","creation":"2019-03-27T02:50:46Z"},"accession":"S-EPMC5514894","cross_references":{"pubmed":["28415748"],"doi":["10.18632/oncotarget.16183"]}}