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dc.contributor.authorMarisa Sanchez
dc.contributor.authorYingying Lin
dc.contributor.authorChih-Cheng Yang
dc.contributor.authorPhilip McQuary
dc.contributor.authorAlexandre Rosa Campos
dc.contributor.authorPedro Aza Blanc
dc.contributor.authorDieter A. Wolf
dc.date.accessioned2020-10-10T02:09:24Z
dc.date.available2020-10-10T02:09:24Z
dc.date.issued2019-10-25
dc.identifier.citationiScience,2019,
dc.identifier.other10.1016/j.isci.2019.09.031
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/174864
dc.description.abstractSummary(#br)The cellular stress response triggers a cascade of events leading to transcriptional reprogramming and a transient inhibition of global protein synthesis, which is thought to be mediated by phosphorylation of eukaryotic initiation factor-2α (eIF2α). Using mouse embryonic fibroblasts (MEFs) and the fission yeast S. pombe, we report that rapid translational arrest and cell survival in response to hydrogen peroxide-induced oxidative stress do not rely on eIF2α kinases and eIF2α phosphorylation. Rather H 2 O 2 induces a block in elongation through phosphorylation of eukaryotic elongation factor 2 (eEF2). Kinetic and dose-response analyses uncovered crosstalk between the eIF2α and eEF2 phosphorylation pathways, indicating that, in MEFs, eEF2 phosphorylation initiates the acute shutdown in translation, which is maintained by eIF2α phosphorylation. Our results challenge the common conception that eIF2α phosphorylation is the primary trigger of translational arrest in response to oxidative stress and point to integrated control that may facilitate the survival of cancer cells.
dc.language.isozh_CN
dc.subjectBiological Sciences
dc.subjectMolecular Biology
dc.subjectMolecular Mechanism of Gene Regulation
dc.subjectMolecular Microbiology
dc.subjectCell Biology
dc.titleCross Talk between eIF2α and eEF2 Phosphorylation Pathways Optimizes Translational Arrest in Response to Oxidative Stress
dc.typeArticle


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