Evidence map›Paper›PMID 31980815›Full record

ArticleNucleic acids research2020

Cooperation of the NEIL3 and Fanconi anemia/BRCA pathways in interstrand crosslink repair.

Niu Li, Jian Wang, Susan S Wallace, Jing Chen, Jia Zhou, Alan D D'Andrea

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
    Review
  8. Review
  9. Review
  10. Structure andmBio · 2024
    Article
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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

6 authors at 4 institutions in 2 countries.

Niu LiDepartment of Medical Genetics and Molecular Diagnostic Laboratory, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jian WangDepartment of Medical Genetics and Molecular Diagnostic Laboratory, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Susan S WallaceDepartment of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT, USA.
Jing ChenKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology and Oncology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jia ZhouDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Alan D D'AndreaDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Harvard University · USShanghai Children's Medical Center · CNShanghai Jiao Tong University · CNUniversity of Vermont · US

Funding

Xenograft CoreP01HL048546 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI GROMPE, MARKUS · 1994 to 2020
$36.4M
Molecular Pathogenesis of Fanconi AnemiaR37HL052725 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN D. · 2004 to 2013
$3.9M
NHLBI NIH HHS P01 HL048546NHLBI NIH HHS R37 HL052725
6 · The paper itself

Abstract

The NEIL3 DNA glycosylase is a base excision repair enzyme that excises bulky base lesions from DNA. Although NEIL3 has been shown to unhook interstrand crosslinks (ICL) in Xenopus extracts, how NEIL3 participants in ICL repair in human cells and its corporation with the canonical Fanconi anemia (FA)/BRCA pathway remain unclear. Here we show that the NEIL3 and the FA/BRCA pathways are non-epistatic in psoralen-ICL repair. The NEIL3 pathway is the major pathway for repairing psoralen-ICL, and the FA/BRCA pathway is only activated when NEIL3 is not present. Mechanistically, NEIL3 is recruited to psoralen-ICL in a rapid, PARP-dependent manner. Importantly, the NEIL3 pathway repairs psoralen-ICLs without generating double-strand breaks (DSBs), unlike the FA/BRCA pathway. In addition, we found that the RUVBL1/2 complex physically interact with NEIL3 and function within the NEIL3 pathway in psoralen-ICL repair. Moreover, TRAIP is important for the recruitment of NEIL3 but not FANCD2, and knockdown of TRAIP promotes FA/BRCA pathway activation. Interestingly, TRAIP is non-epistatic with both NEIL3 and FA pathways in psoralen-ICL repair, suggesting that TRAIP may function upstream of the two pathways. Taken together, the NEIL3 pathway is the major pathway to repair psoralen-ICL through a unique DSB-free mechanism in human cells.

Indexed as

AnimalsATPases Associated with Diverse Cellular ActivitiesCarrier ProteinsDNA Breaks, Double-StrandedDNA DamageDNA HelicasesDNA RepairDNA ReplicationFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinFibroblastsFicusinHeLa CellsHumansN-Glycosyl HydrolasesProtein BindingATPases Associated with Diverse Cellular ActivitiesCarrier ProteinsDNA HelicasesFANCA protein, humanFANCD2 protein, humanFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinFicusinNEIL3 protein, humanN-Glycosyl HydrolasesRUVBL1 protein, humanRUVBL2 protein, humanTRAIP protein, humanUbiquitin-Protein Ligases

Identifiers

PMID31980815
PMCPMC7102959
OpenAlexW3002698677

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.