Dicer promotes transcription termination at sites of replication stress to maintain genome stability.

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Published in Cell on October 16, 2014

Authors

Stephane E Castel1, Jie Ren1, Sonali Bhattacharjee1, An-Yun Chang2, Mar Sánchez3, Alberto Valbuena3, Francisco Antequera3, Robert A Martienssen4

Author Affiliations

1: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, NY 11794, USA.
3: Instituto de Biología Funcional y Genómica, CSIC/Universidad de Salamanca, Salamanca 37007, Spain.
4: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, NY 11794, USA. Electronic address: martiens@cshl.edu.

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