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Fanconi anemia proteins participate in a break-induced-replication-like pathway to counter replication stress

Authors
  • Xu, Xinlin1
  • Xu, Yixi1, 2
  • Guo, Ruiyuan1
  • Xu, Ran1
  • Fu, Congcong1
  • Xing, Mengtan1, 3
  • Sasanuma, Hiroyuki4
  • Li, Qing1
  • Takata, Minoru4
  • Takeda, Shunichi4
  • Guo, Rong1
  • Xu, Dongyi1
  • 1 Peking University, Beijing, China , Beijing (China)
  • 2 Westlake University, Hangzhou, Zhejiang, China , Zhejiang (China)
  • 3 Shanghai East Hospital, School of Life Science and Technology, Shanghai Key Laboratory of Signaling and Disease Research, Tongji University, Shanghai, China , Shanghai (China)
  • 4 Kyoto University, Kyoto, Japan , Kyoto (Japan)
Type
Published Article
Journal
Nature Structural & Molecular Biology
Publisher
Springer Nature
Publication Date
Jun 10, 2021
Volume
28
Issue
6
Pages
487–500
Identifiers
DOI: 10.1038/s41594-021-00602-9
Source
Springer Nature
Disciplines
  • article
License
Yellow

Abstract

Cell-based, in vitro and in vivo assays reveal that Fanconi anemia factors function in a BRCA1-dependent BIR-like pathway to restart stalled replication forks and that persistent replication stress contributes to FA pathogenesis.

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