Evidence map›Paper›PMID 31796734›Full record

ArticleNature communications2019

Barrier-to-autointegration factor 1 (Banf1) regulates poly [ADP-ribose] polymerase 1 (PARP1) activity following oxidative DNA damage.

Emma Bolderson, Joshua T Burgess, Jun Li, Neha S Gandhi, Didier Boucher, Laura V Croft, Samuel Beard, Jennifer J Plowman, Amila Suraweera, Mark N Adams and 5 more

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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.7field-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

45 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025
    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

15 authors at 5 institutions in 4 countries.

Emma BoldersonCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia. emma.bolderson@qut.edu.au.ORCID http://orcid.org/0000-0002-2849-1177
Joshua T BurgessCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Jun LiDepartment of Genetics, Paul F. Glenn Center for Biology of Aging Research, Harvard Medical School, Boston, MA, 02115, USA.
Neha S GandhiSchool of Mathematical Sciences, Queensland University of Technology, Brisbane, 4000, Queensland, Australia.ORCID http://orcid.org/0000-0003-3119-6731
Didier BoucherCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Laura V CroftCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Samuel BeardCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Jennifer J PlowmanCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Amila SuraweeraCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.ORCID http://orcid.org/0000-0002-1079-2887
Mark N AdamsCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.ORCID http://orcid.org/0000-0003-1906-5018
Ali NaqiCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Shu-Dong ZhangNorthern Ireland Centre for Stratified Medicine, University of Ulster, Londonderry, UK.ORCID http://orcid.org/0000-0002-7721-0167
David A SinclairDepartment of Genetics, Paul F. Glenn Center for Biology of Aging Research, Harvard Medical School, Boston, MA, 02115, USA.
Kenneth J O'ByrneCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia.
Derek J RichardCancer & Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute (TRI), Queensland University of Technology (QUT), Brisbane, Queensland, Australia. derek.richard@qut.edu.au.
Translational Research Institute · AUHarvard University · USPennsylvania State University · USQueensland University of Technology · AUUniversity of Ulster · GB

Funding

Uncovering the Human SecretomeDP1AG058605 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2017 to 2021
$5.9M
Role of Sgs1 DNA helicase in telomere maintenanceR01AG019719 · NIA · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SINCLAIR, DAVID A. · 2001 to 2022
$5.3M
SIRT1 as a regulator of health and lifespan of mammalsR37AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2012 to 2021
$4.1M
Elucidating mechanisms of SIRT1 activationR01DK100263 · NIDDK · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2016 to 2020
$2.5M
NIA NIH HHS DP1 AG058605NIA NIH HHS R01 AG019719NIA NIH HHS R37 AG028730NIDDK NIH HHS R01 DK100263
6 · The paper itself

Abstract

The DNA repair capacity of human cells declines with age, in a process that is not clearly understood. Mutation of the nuclear envelope protein barrier-to-autointegration factor 1 (Banf1) has previously been shown to cause a human progeroid disorder, Néstor-Guillermo progeria syndrome (NGPS). The underlying links between Banf1, DNA repair and the ageing process are unknown. Here, we report that Banf1 controls the DNA damage response to oxidative stress via regulation of poly [ADP-ribose] polymerase 1 (PARP1). Specifically, oxidative lesions promote direct binding of Banf1 to PARP1, a critical NAD

Indexed as

DNA DamageOxidative StressCell Line, TumorDNA-Binding ProteinsHEK293 CellsHumansMutationPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1ProgeriaProtein BindingProtein DomainsBANF1 protein, humanDNA-Binding ProteinsPARP1 protein, humanPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1

Identifiers

PMID31796734
PMCPMC6890647
OpenAlexW2993868505

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.