Evidence map›Paper›PMID 30831436›Full record

ReviewDNA repair2019

Role of deubiquitinases in DNA damage response.

John Le, Eric Perez, Leah Nemzow, Feng Gong

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Role of Deubiquitinases in Human Cancers: Potential Targeted Therapy.International journal of molecular sciences · 2020
    Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

John LeDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, United States.
Eric PerezDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, United States.
Leah NemzowDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, United States.
Feng GongDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, United States. Electronic address: fgong@med.miami.edu.
University of Miami · US

Funding

SWI/SNF chromatin remodeling in nucleotide excision repairR01ES017784 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GONG, FENG · 2010 to 2014
$1.7M
Novel deubiquitinating activities targeting DNA damage recognition in NERR21ES024882 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GONG, FENG · 2015 to 2016
$422k
NIEHS NIH HHS R01 ES017784NIEHS NIH HHS R21 ES024882
6 · The paper itself

Abstract

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.

Indexed as

DNA DamageDeubiquitinating EnzymesDNA RepairFanconi AnemiaHumansDeubiquitinating EnzymesDeubiquitinationDNA damage responseDNA repairPost-transcriptional modification

Identifiers

PMID30831436
PMCPMC6561784
OpenAlexW2917884512

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.