Evidence map›Paper›PMID 26695548›Full record

ArticleOncotarget2016

Replication stress induced site-specific phosphorylation targets WRN to the ubiquitin-proteasome pathway.

Fengtao Su, Souparno Bhattacharya, Salim Abdisalaam, Shibani Mukherjee, Hirohiko Yajima, Yanyong Yang, Ritu Mishra, Kalayarasan Srinivasan, Subroto Ghose, David J Chen and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. 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
2.0field-weighted citation impact, top 14% 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, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Werner Syndrome Protein and DNA Replication.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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

12 authors at 2 institutions in 1 country.

Fengtao SuDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Souparno BhattacharyaDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Salim AbdisalaamDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Shibani MukherjeeDepartment of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Hirohiko YajimaDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Yanyong YangDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Ritu MishraDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Kalayarasan SrinivasanDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Subroto GhoseDepartment of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
David J ChenDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Steven M YannoneLife Science Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA.
Aroumougame AsaithambyDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The University of Texas Southwestern Medical Center · USLawrence Berkeley National Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Faithful and complete genome replication in human cells is essential for preventing the accumulation of cancer-promoting mutations. WRN, the protein defective in Werner syndrome, plays critical roles in preventing replication stress, chromosome instability, and tumorigenesis. Herein, we report that ATR-mediated WRN phosphorylation is needed for DNA replication and repair upon replication stress. A serine residue, S1141, in WRN is phosphorylated in vivo by the ATR kinase in response to replication stress. ATR-mediated WRN S1141 phosphorylation leads to ubiquitination of WRN, facilitating the reversible interaction of WRN with perturbed replication forks and subsequent degradation of WRN. The dynamic interaction between WRN and DNA is required for the suppression of new origin firing and Rad51-dependent double-stranded DNA break repair. Significantly, ATR-mediated WRN phosphorylation is critical for the suppression of chromosome breakage during replication stress. These findings reveal a unique role for WRN as a modulator of DNA repair, replication, and recombination, and link ATR-WRN signaling to the maintenance of genome stability.

Indexed as

DNA ReplicationSignal TransductionAtaxia Telangiectasia Mutated ProteinsBinding SitesBlotting, WesternCell Line, TumorCells, CulturedDNA DamageDNA RepairExodeoxyribonucleasesFluorescence Recovery After PhotobleachingHeLa CellsHumansMicroscopy, ConfocalPhosphorylationProteasome Endopeptidase ComplexAtaxia Telangiectasia Mutated ProteinsATR protein, humanExodeoxyribonucleasesProteasome Endopeptidase ComplexRecQ HelicasesSerineUbiquitinsWerner Syndrome HelicaseWRN protein, humanchromosome instabilityGerotargetpost-translational modificationreplication stressWerner syndromeWerner syndrome protein

Identifiers

PMID26695548
PMCPMC4807982
OpenAlexW2214203291

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.