Evidence map›Paper›PMID 31619012›Full record

ArticleCells2019

WIP1 Promotes Homologous Recombination and Modulates Sensitivity to PARP Inhibitors.

Kamila Burdova, Radka Storchova, Matous Palek, Libor Macurek

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  6. Review
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  9. eLife · 2024
    Article
  10. bioRxiv : the preprint server for biology · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
  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

4 authors at 1 institution in 1 country.

Kamila BurdovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, CZ14220 Prague, Czech Republic. kamila.burdova@img.cas.cz.
Radka StorchovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, CZ14220 Prague, Czech Republic. radka.storchova@img.cas.cz.
Matous PalekCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, CZ14220 Prague, Czech Republic. matous.palek@img.cas.cz.
Libor MacurekCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, CZ14220 Prague, Czech Republic. libor.macurek@img.cas.cz.ORCID 0000-0002-0987-1238
Czech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genotoxic stress triggers a combined action of DNA repair and cell cycle checkpoint pathways. Protein phosphatase 2C delta (referred to as WIP1) is involved in timely inactivation of DNA damage response by suppressing function of p53 and other targets at chromatin. Here we show that WIP1 promotes DNA repair through homologous recombination. Loss or inhibition of WIP1 delayed disappearance of the ionizing radiation-induced 53BP1 foci in S/G2 cells and promoted cell death. We identify breast cancer associated protein 1 (BRCA1) as interactor and substrate of WIP1 and demonstrate that WIP1 activity is needed for correct dynamics of BRCA1 recruitment to chromatin flanking the DNA lesion. In addition, WIP1 dephosphorylates 53BP1 at Threonine 543 that was previously implicated in mediating interaction with RIF1. Finally, we report that inhibition of WIP1 allowed accumulation of DNA damage in S/G2 cells and increased sensitivity of cancer cells to a poly-(ADP-ribose) polymerase inhibitor olaparib. We propose that inhibition of WIP1 may increase sensitivity of BRCA1-proficient cancer cells to olaparib.

Indexed as

Antineoplastic AgentsApoptosisBRCA1 ProteinBreast NeoplasmsCell Line, TumorCell ProliferationChromatinDNA DamageDNA RepairDrug Resistance, NeoplasmG2 Phase Cell Cycle CheckpointsHEK293 CellsHomologous RecombinationHumansPhthalazinesPiperazinesAntineoplastic AgentsBRCA1 ProteinBRCA1 protein, humanChromatinolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsPPM1D protein, humanProtein Phosphatase 2CTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1chemotherapyDNA repairgenotoxic stressolaparibPARP inhibitorphosphatase

Identifiers

PMID31619012
PMCPMC6830099
OpenAlexW2981019988

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.