Evidence map›Paper›PMID 31253762›Full record

ArticleNature communications2019

DNA requirement in FANCD2 deubiquitination by USP1-UAF1-RAD51AP1 in the Fanconi anemia DNA damage response.

Fengshan Liang, Adam S Miller, Simonne Longerich, Caroline Tang, David Maranon, Elizabeth A Williamson, Robert Hromas, Claudia Wiese, Gary M Kupfer, Patrick Sung

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Phosphoregulation of RAD51AP1 function in homology-directed repair.bioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. ATAD5 functions as a regulatory platform for Ub-PCNA deubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

10 authors at 3 institutions in 1 country.

Fengshan LiangDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT, USA.
Adam S MillerDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT, USA.
Simonne LongerichDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT, USA.
Caroline TangDepartment of Pediatrics, Section of Hematology-Oncology, Yale University School of Medicine, New Haven, CT, USA.
David MaranonDepartment of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO, USA.
Elizabeth A WilliamsonDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Robert HromasDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Claudia WieseDepartment of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO, USA.
Gary M KupferDepartment of Pediatrics, Section of Hematology-Oncology, Yale University School of Medicine, New Haven, CT, USA. gary.kupfer@yale.edu.
Patrick SungDepartment of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT, USA. sungp@uthscsa.edu.
Yale University · USThe University of Texas Health Science Center at San Antonio · USColorado State University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Yale Cooperative Hematology Specialized Core CenterU54DK106857 · NIDDK · YALE UNIVERSITY · PI JOHN HWA, Diane S Krause · 2015 to 2026
$9.7M
YEAST DNA REPAIR GENES AND PROTEINS OF THE RAD52 GROUPR01ES007061 · NIEHS · YALE UNIVERSITY · PI Patrick Sung · 1995 to 2026
$9.4M
Mechanistic Dissection of the Fanconi Anemia Pathway of DNA Damage Response and RR01CA168635 · NCI · YALE UNIVERSITY · PI Gary M Kupfer, Patrick Sung · 2013 to 2026
$5.8M
EEPD1 Repair of Stressed Replication ForksR01CA205224 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robert A Hromas · 2016 to 2026
$3.3M
Genome Maintenance via the BRCA-PALB2 Tumor Suppressor NetworkR01CA220123 · NCI · YALE UNIVERSITY · PI SUNG, PATRICK · 2017 to 2019
$1.2M
Mechanisms for Chromosomal TranslocationsR01GM109645 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HROMAS, ROBERT A · 2015 to 2018
$1.2M
NCATS NIH HHS UL1 TR001863NCI NIH HHS P01 CA092584NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA168635NCI NIH HHS R01 CA205224NCI NIH HHS R01 CA220123NIDDK NIH HHS U54 DK106857NIEHS NIH HHS R01 ES007061NIGMS NIH HHS R01 GM109645U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1 CA168635U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1 CA205224U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1 CA220123U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1 ES007061U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1 GM109645
6 · The paper itself

Abstract

Fanconi anemia (FA) is a multigenic disease of bone marrow failure and cancer susceptibility stemming from a failure to remove DNA crosslinks and other chromosomal lesions. Within the FA DNA damage response pathway, DNA-dependent monoubiquitinaton of FANCD2 licenses downstream events, while timely FANCD2 deubiquitination serves to extinguish the response. Here, we show with reconstituted biochemical systems, which we developed, that efficient FANCD2 deubiquitination by the USP1-UAF1 complex is dependent on DNA and DNA binding by UAF1. Surprisingly, we find that the DNA binding activity of the UAF1-associated protein RAD51AP1 can substitute for that of UAF1 in FANCD2 deubiquitination in our biochemical system. We also reveal the importance of DNA binding by UAF1 and RAD51AP1 in FANCD2 deubiquitination in the cellular setting. Our results provide insights into a key step in the FA pathway and help define the multifaceted role of the USP1-UAF1-RAD51AP1 complex in DNA damage tolerance and genome repair.

Indexed as

DNADNA-Binding ProteinsDNA DamageFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinGene Expression RegulationHumansMutationNuclear ProteinsProtein BindingRNA-Binding ProteinsUbiquitinationUbiquitin-Specific ProteasesDNADNA-Binding ProteinsFanconi Anemia Complementation Group D2 ProteinNuclear ProteinsRAD51AP1 protein, humanRNA-Binding ProteinsUbiquitin-Specific ProteasesUSP1 protein, humanWDR48 protein, human

Identifiers

PMID31253762
PMCPMC6599204
OpenAlexW2955745836

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.