Evidence map›Paper›PMID 26549024›Full record

ArticleOncogene2016

RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress.

N Kanu, T Zhang, R A Burrell, A Chakraborty, J Cronshaw, C DaCosta, E Grönroos, H N Pemberton, E Anderton, L Gonzalez and 4 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. The function of Mgs1/WRNIP1 in genome maintenance.Frontiers in molecular biosciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 4 countries.

N KanuMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
T ZhangMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
R A BurrellTranslational Cancer Therapeutics Laboratory, The Francis Crick Institute, London, UK.
A ChakrabortyMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
J CronshawMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
C DaCostaMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
E GrönroosTranslational Cancer Therapeutics Laboratory, The Francis Crick Institute, London, UK.
H N PembertonMolecular Oncology Laboratory, The Francis Crick Institute, London, UK.
E AndertonMolecular Oncology Laboratory, The Francis Crick Institute, London, UK.
L GonzalezDNA Damage Tolerance Laboratory, The Francis Crick Institute, London, UK.
S SabbionedaIstituto di Genetica Molecolare-CNR, Pavia, Italy.
H D UlrichDNA Damage Tolerance Laboratory, The Francis Crick Institute, London, UK.
C SwantonTranslational Cancer Therapeutics Laboratory, The Francis Crick Institute, London, UK.
A BehrensMammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
The Francis Crick Institute · GBUniversity College London · GBInstitute of Molecular Biology · DEIstituto di Genetica Molecolare · ITKing's College London · GB

Funding

Cancer Research UK 15679Cancer Research UK A15679Cancer Research UK A3588European Research Council 281661
6 · The paper itself

Abstract

The DNA replication machinery invariably encounters obstacles that slow replication fork progression, and threaten to prevent complete replication and faithful segregation of sister chromatids. The resulting replication stress activates ATR, the major kinase involved in resolving impaired DNA replication. In addition, replication stress also activates the related kinase ATM, which is required to prevent mitotic segregation errors. However, the molecular mechanism of ATM activation by replication stress is not defined. Here, we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts with the ATM cofactor ATMIN via WRN-interacting protein 1 (WRNIP1). ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation. Thus, WRNIP1 connects PCNA monoubiquitination with ATMIN/ATM to activate ATM signalling in response to replication stress and contribute to the maintenance of genomic stability.

Indexed as

DNA ReplicationAphidicolinAtaxia Telangiectasia Mutated ProteinsATPases Associated with Diverse Cellular ActivitiesCarrier ProteinsDNA-Binding ProteinsDNA DamageGenomic InstabilityHumansProliferating Cell Nuclear AntigenSignal TransductionTranscription FactorsUbiquitinationUbiquitin-Protein LigasesAphidicolinAtaxia Telangiectasia Mutated ProteinsATMIN protein, humanATM protein, humanATPases Associated with Diverse Cellular ActivitiesCarrier ProteinsDNA-Binding ProteinsProliferating Cell Nuclear AntigenRAD18 protein, humanTranscription FactorsUbiquitin-Protein LigasesWRNIP1 protein, human

Identifiers

PMID26549024
PMCPMC4842010
OpenAlexW2340594125

What OpenQuestion holds

Textmetadata
LicenceTDM
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.