作者: Abdelghani Mazouzi , Alexey Stukalov , André C. Müller , Doris Chen , Marc Wiedner
DOI: 10.1016/J.CELREP.2016.03.077
关键词:
摘要: The cellular response to replication stress requires the DNA-damage-responsive kinase ATM and its cofactor ATMIN; however, roles of this signaling pathway following are unclear. To identify functions ATMIN in stress, we utilized both transcriptomics quantitative mass-spectrometry-based phosphoproteomics. We found that induced by aphidicolin triggered widespread changes gene expression protein phosphorylation patterns. These gave rise distinct early late responses. Furthermore, our analysis revealed previously unknown targets downstream stress. demonstrate ATMIN-dependent H2AX CRMP2, a implicated Alzheimer's disease but not DNA damage response. Overall, dataset provides comprehensive resource for discovering responses and, potentially, associated pathologies.