Evidence map›Paper›PMID 28854357›Full record

ArticleCell reports2017

NEIL3 Repairs Telomere Damage during S Phase to Secure Chromosome Segregation at Mitosis.

Jia Zhou, Jany Chan, Marie Lambelé, Timur Yusufzai, Jason Stumpff, Patricia L Opresko, Markus Thali, Susan S Wallace

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023
    Review
  15. PromotersRSC chemical biology · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Jia ZhouDepartment of Microbiology and Molecular Genetics, College of Medicine and College of Agriculture and Life Sciences, University of Vermont, Burlington, VT 05405, USA; Graduate Program in Cell and Molecular Biology, University of Vermont, Burlington, VT 05405, USA; Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Jany ChanDepartment of Microbiology and Molecular Genetics, College of Medicine and College of Agriculture and Life Sciences, University of Vermont, Burlington, VT 05405, USA.
Marie LambeléDepartment of Microbiology and Molecular Genetics, College of Medicine and College of Agriculture and Life Sciences, University of Vermont, Burlington, VT 05405, USA.
Timur YusufzaiDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Jason StumpffDepartment of Molecular Physiology and Biophysics, College of Medicine, University of Vermont, Burlington, VT 05405, USA; Graduate Program in Cell and Molecular Biology, University of Vermont, Burlington, VT 05405, USA.
Patricia L OpreskoDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, Hillman Cancer Center, Pittsburgh, PA 15213, USA.
Markus ThaliDepartment of Microbiology and Molecular Genetics, College of Medicine and College of Agriculture and Life Sciences, University of Vermont, Burlington, VT 05405, USA; Graduate Program in Cell and Molecular Biology, University of Vermont, Burlington, VT 05405, USA. Electronic address: markus.thali@uvm.edu.
Susan S WallaceDepartment of Microbiology and Molecular Genetics, College of Medicine and College of Agriculture and Life Sciences, University of Vermont, Burlington, VT 05405, USA; Graduate Program in Cell and Molecular Biology, University of Vermont, Burlington, VT 05405, USA. Electronic address: susan.wallace@uvm.edu.
University of Vermont · USHarvard University · USUPMC Hillman Cancer Center · US

Funding

SUBSTRATE SPECIFICITY OF THE BER OXIDATIVE DNA GLYCOSYLASESP01CA098993 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI DOUBLIE, SYLVIE · 2004 to 2021
$25.9M
Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Molecular regulation of HIV-1 assembly, release and cell-to-cell transmissionR01AI080302 · NIAID · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI THALI, MARKUS · 2009 to 2013
$1.9M
Multiscale analysis of HIV-1 assembly, release, and cell-to-cell transmissionR01GM117839 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI THALI, MARKUS · 2015 to 2018
$1.6M
Mechanisms of Telomere Resistance to DNA Lesion RemovalR01ES022944 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L · 2013 to 2017
$1.6M
NCI NIH HHS P01 CA098993NIAID NIH HHS R01 AI080302NIEHS NIH HHS R01 ES022944NIGMS NIH HHS P20 GM103496NIGMS NIH HHS R01 GM117839
6 · The paper itself

Abstract

Oxidative damage to telomere DNA compromises telomere integrity. We recently reported that the DNA glycosylase NEIL3 preferentially repairs oxidative lesions in telomere sequences in vitro. Here, we show that loss of NEIL3 causes anaphase DNA bridging because of telomere dysfunction. NEIL3 expression increases during S phase and reaches maximal levels in late S/G2. NEIL3 co-localizes with TRF2 and associates with telomeres during S phase, and this association increases upon oxidative stress. Mechanistic studies reveal that NEIL3 binds to single-stranded DNA via its intrinsically disordered C terminus in a telomere-sequence-independent manner. Moreover, NEIL3 is recruited to telomeres through its interaction with TRF1, and this interaction enhances the enzymatic activity of purified NEIL3. Finally, we show that NEIL3 interacts with AP Endonuclease 1 (APE1) and the long-patch base excision repair proteins PCNA and FEN1. Taken together, we propose that NEIL3 protects genome stability through targeted repair of oxidative damage in telomeres during S/G2 phase.

Indexed as

Chromosome SegregationDNA DamageDNA RepairMitosisS PhaseCD4-Positive T-LymphocytesCell Cycle CheckpointsCell NucleusDNAGene Knockdown TechniquesHCT116 CellsHeLa CellsHumansMicrotubulesN-Glycosyl HydrolasesOxidative StressDNANEIL3 protein, humanN-Glycosyl HydrolasesDNA repairmitotic defectsNEIL3 glycosylasetelomere

Identifiers

PMID28854357
PMCPMC5606162
OpenAlexW2751221573

What OpenQuestion holds

Textmetadata
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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.