Evidence map›Paper›PMID 27463890›Full record

ArticleCell cycle (Georgetown, Tex.)2016

The USP1-UAF1 complex interacts with RAD51AP1 to promote homologous recombination repair.

Scott Cukras, Euiho Lee, Emily Palumbo, Pamela Benavidez, George-Lucian Moldovan, Younghoon Kee

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  8. Review
  9. SUMO and the DNA damage response.Biochemical Society transactions · 2024
    Review
  10. Review
  11. Article
  12. Deubiquitinating Enzyme USP12 Regulates the Pro-Apoptosis Protein Bax.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Scott Cukrasa Department of Cell Biology , Microbiology, and Molecular Biology, College of Arts and Sciences, University of South Florida , Tampa , FL , USA.
Euiho Leea Department of Cell Biology , Microbiology, and Molecular Biology, College of Arts and Sciences, University of South Florida , Tampa , FL , USA.
Emily Palumboa Department of Cell Biology , Microbiology, and Molecular Biology, College of Arts and Sciences, University of South Florida , Tampa , FL , USA.
Pamela Benavideza Department of Cell Biology , Microbiology, and Molecular Biology, College of Arts and Sciences, University of South Florida , Tampa , FL , USA.
George-Lucian Moldovanb Department of Biochemistry and Molecular Biology , Pennsylvania State University College of Medicine , Hershey , PA , USA.
Younghoon Keea Department of Cell Biology , Microbiology, and Molecular Biology, College of Arts and Sciences, University of South Florida , Tampa , FL , USA.
University of South Florida · USPennsylvania State University · US

Funding

Function and Regulation of the Fanconi Anemia pathway in DNA repairR15HL126113 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI KEE, YOUNGHOON · 2015 to 2015
$440k
NHLBI NIH HHS R15 HL126113
6 · The paper itself

Abstract

USP1 deubiquitinating enzyme and its stoichiometric binding partner UAF1 play an essential role in promoting DNA homologous recombination (HR) repair in response to various types of DNA damaging agents. Deubiquitination of FANCD2 may be attributed to the key role of USP1-UAF1 complex in regulating HR repair, however whether USP1-UAF1 promotes HR repair independently of FANCD2 deubiquitination is not known. Here we show evidence that the USP1-UAF1 complex has a FANCD2-independent function in promoting HR repair. Proteomic search of UAF1-interacting proteins revealed that UAF1 associates with RAD51AP1, a RAD51-interacting protein implicated in HR repair. We show that UAF1 mediates the interaction between USP1 and RAD51AP1, and that depletion of USP1 or UAF1 led to a decreased stability of RAD51AP1. Protein interaction mapping analysis identified some key residues within RAD51AP1 required for interacting with the USP1-UAF1 complex. Cells expressing the UAF1 interaction-deficient mutant of RAD51AP1 show increased chromosomal aberrations in response to Mitomycin C treatment. Moreover, similar to the RAD51AP1 depleted cells, the cells expressing UAF1-interaction deficient RAD51AP1 display persistent RAD51 foci following DNA damage exposure, indicating that these factors regulate a later step during the HR repair. These data altogether suggest that the USP1-UAF1 complex promotes HR repair via multiple mechanisms: through FANCD2 deubiquitination, as well as by interacting with RAD51AP1.

Indexed as

Recombinational DNA RepairDNA-Binding ProteinsGene DeletionGene Knockdown TechniquesHeLa CellsHumansMutant ProteinsNuclear ProteinsPhenotypeProtein BindingProtein Interaction MappingProtein StabilityRNA-Binding ProteinsUbiquitin-Specific ProteasesDNA-Binding ProteinsMutant ProteinsNuclear ProteinsRAD51AP1 protein, humanRNA-Binding ProteinsUbiquitin-Specific ProteasesUSP1 protein, humanWDR48 protein, humandeubiquitinating enzymehomologous recombination repairRAD51AP1UAF1USP1

Identifiers

PMID27463890
PMCPMC5053553
OpenAlexW2488348433

What OpenQuestion holds

Textmetadata
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.