首页> Nature communications> SLFN11 counteracts the RFWD3-PRIMPOL DNA damage tolerance axis to restrain gapped DNA synthesis in response to replication stress.

SLFN11 counteracts the RFWD3-PRIMPOL DNA damage tolerance axis to restrain gapped DNA synthesis in response to replication stress.

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第一作者： Kate E,Coleman

第一单位： Department of Biochemistry & Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA.

作者： Kate E,Coleman ^[1] ; Dong-Woo,Shin ^[2] ; Liana,Goehring ^[3] ; Beata,Szeitz ^[4] ; David,Fenyö ^[4] ; Eli,Rothenberg ^[1] ; John T,Poirier ^[5] ; Tony T,Huang ^[6]

作者单位： Department of Biochemistry & Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA. ^[1] Vilcek Institute of Graduate Biomedical Sciences, NYU Grossman School of Medicine, New York, USA. ^[2] Department of Biochemistry & Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA.;Vilcek Institute of Graduate Biomedical Sciences, NYU Grossman School of Medicine, New York, USA. ^[3] Department of Biochemistry & Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA.;Institute for Systems Genetics, New York University Grossman School of Medicine, New York, NY, USA. ^[4] Department of Medicine, Laura and Isaac Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, NY, USA. John.Poirier@nyulangone.org.;Laura and Isaac Perlmutter Cancer Center, New York University Langone Health, New York, NY, USA. John.Poirier@nyulangone.org. ^[5] Department of Biochemistry & Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA. Tony.huang@nyulangone.org. ^[6]