Evidence map›Paper›PMID 29968717›Full record

ArticleNature communications2018

A senataxin-associated exonuclease SAN1 is required for resistance to DNA interstrand cross-links.

Alex M Andrews, Heather J McCartney, Tim M Errington, Alan D D'Andrea, Ian G Macara

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. 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
1.0field-weighted citation impact, top 24% 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, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Role of Senataxin in Amyotrophic Lateral Sclerosis.Journal of molecular neuroscience : MN · 2023
    Review
  6. Review
  7. Review
  8. Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023
    Review
  9. Article
  10. Article
  11. Integrated genome and transcriptome analyses reveal the mechanism of genome instability in ataxia with oculomotor apraxia 2.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. DNA damage and repair in the hematopoietic system.Acta biochimica et biophysica Sinica · 2022
    Review
  13. Observational
  14. Review
  15. Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.Progress in biophysics and molecular biology · 2020
    Review
  16. Review
  17. Article
  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

5 authors at 3 institutions in 1 country.

Alex M AndrewsDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, 37215, USA.
Heather J McCartneyDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, 37215, USA.
Tim M ErringtonDepartment of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA, 22908, USA.ORCID http://orcid.org/0000-0002-4959-5143
Alan D D'AndreaDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, 02215, USA.
Ian G MacaraDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, 37215, USA. ian.g.macara@vanderbilt.edu.
Vanderbilt University · USCenter for Open Science · USHarvard University · US

Funding

Cancer and ContextR35CA197571 · NCI · VANDERBILT UNIVERSITY · PI MACARA, IAN G · 2015 to 2021
$6.7M
The RAN GTPaseR01GM050526 · NIGMS · VANDERBILT UNIVERSITY · PI MACARA, IAN G · 1994 to 2014
$4.8M
NCI NIH HHS R35 CA197571NIGMS NIH HHS R01 GM050526U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R35 CA197571
6 · The paper itself

Abstract

Interstrand DNA cross-links (ICLs) block both replication and transcription, and are commonly repaired by the Fanconi anemia (FA) pathway. However, FA-independent repair mechanisms of ICLs remain poorly understood. Here we report a previously uncharacterized protein, SAN1, as a 5' exonuclease that acts independently of the FA pathway in response to ICLs. Deletion of SAN1 in HeLa cells and mouse embryonic fibroblasts causes sensitivity to ICLs, which is prevented by re-expression of wild type but not nuclease-dead SAN1. SAN1 deletion causes DNA damage and radial chromosome formation following treatment with Mitomycin C, phenocopying defects in the FA pathway. However, SAN1 deletion is not epistatic with FANCD2, a core FA pathway component. Unexpectedly, SAN1 binds to Senataxin (SETX), an RNA/DNA helicase that resolves R-loops. SAN1-SETX binding is increased by ICLs, and is required to prevent cross-link sensitivity. We propose that SAN1 functions with SETX in a pathway necessary for resistance to ICLs.

Indexed as

AnimalsDNA DamageDNA HelicasesDNA RepairEnzyme AssaysExodeoxyribonucleasesFanconi Anemia Complementation Group D2 ProteinFemaleFibroblastsGene Knockdown TechniquesGene Knockout TechniquesHEK293 CellsHeLa CellsHumansMaleMiceDNA HelicasesExodeoxyribonucleasesFAM120B protein, humanFam120b protein, mouseFANCD2 protein, humanFancd2 protein, mouseFanconi Anemia Complementation Group D2 ProteinMultifunctional EnzymesRecombinant ProteinsRNA HelicasesRNA, Small InterferingSETX protein, humanSETX protein, mouseTrans-Activators

Identifiers

PMID29968717
PMCPMC6030175
OpenAlexW2810799927

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.