Role of deubiquitinases in DNA damage response

John Le, Eric Perez, Leah Nemzow, Feng Gong

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


DNA damage response (DDR) serves as an integrated cellular network to detect cellular stress and react by activating pathways responsible for halting cell cycle progression, stimulating DNA damage repair, and initiating apoptosis. Efficient DDR protects cells from genomic instability while defective DDR can allow DNA lesions to go unrepaired, causing permanent mutations that will affect future generations of cells and possibly cause disease conditions such as cancer. Therefore, DDR mechanisms must be tightly regulated in order to ensure organismal health and viability. One major way of DDR regulation is ubiquitination, which has been long known to control DDR protein localization, activity, and stability. The reversal of this process, deubiquitination, has more recently come to the forefront of DDR research as an important new angle in ubiquitin-mediated regulation of DDR. As such, deubiquitinases have emerged as key factors in DDR. Importantly, deubiquitinases are attractive small-molecule drug targets due to their well-defined catalytic residues that provide a promising avenue for developing new cancer therapeutics. This review focuses on the emerging roles of deubiquitinases in various DNA repair pathways.

Original languageEnglish (US)
Pages (from-to)89-98
Number of pages10
JournalDNA Repair
StatePublished - Apr 2019


  • DNA damage response
  • DNA repair
  • Deubiquitination
  • Post-transcriptional modification

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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