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Crosstalk between ubiquitin and other post-translational modifications on chromatin during double-strand break repair

Authors
  • Zhao, Yu
  • Brickner, Joshua R.
  • Majid, Mona C.
  • Mosammaparast, Nima1, 2
  • 1 Department of Pathology and Immunology
  • 2 Washington University School of Medicine
Type
Published Article
Journal
Trends in Cell Biology
Publisher
Elsevier
Publication Date
Jan 01, 2014
Identifiers
DOI: 10.1016/j.tcb.2014.01.005
Source
Elsevier
Keywords
License
Unknown

Abstract

The cellular response to DNA double-stranded breaks (DSBs) involves a conserved mechanism of recruitment and activation of numerous proteins involved in this pathway. The events that trigger this response in mammalian cells involve several post-translational modifications, but the role of non-proteasomal ubiquitin signaling is particularly central to this pathway. Recent work has demonstrated that ubiquitination does not act alone, but in concert with other post-translational modifications, including phosphorylation, methylation, acetylation, ADP-ribosylation, and other ubiquitin-like modifiers, particularly SUMOylation. We review novel and exciting crosstalk mechanisms between ubiquitination and other post-translational modifications, many of which work synergistically with each other to activate signaling events and help recruit important DNA damage effector proteins, particularly BRCA1 (breast cancer 1, early onset) and 53BP1 (tumor protein p53 binding protein 1), to sites of DNA damage.

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