Evidence map›Paper›PMID 27819275›Full record

ArticleScientific reports2016

The PTEN phosphatase functions cooperatively with the Fanconi anemia proteins in DNA crosslink repair.

Elizabeth A Vuono, Ananda Mukherjee, David A Vierra, Morganne M Adroved, Charlotte Hodson, Andrew J Deans, Niall G Howlett

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The Impact of Genetic Variants onCold Spring Harbor perspectives in medicine · 2019
    Review
  7. Article
  8. Article
  9. Fanconi anemia protein FANCI functions in ribosome biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Review
  12. Article
  13. 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

7 authors at 4 institutions in 2 countries.

Elizabeth A VuonoDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Ananda MukherjeeDepartment of Obstetrics, Gynecology, and Reproductive Biology, Michigan State University, Grand Rapids, Michigan, USA.
David A VierraDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Morganne M AdrovedDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
Charlotte HodsonGenome Stability Unit, St. Vincent's Institute, Fitzroy, VIC 3065, Australia.
Andrew J DeansGenome Stability Unit, St. Vincent's Institute, Fitzroy, VIC 3065, Australia.
Niall G HowlettDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
University of Rhode Island · USMichigan State University · USSt Vincents Institute of Medical Research · AUUniversity of Melbourne · AU

Funding

Training CoreP20GM103430 · NIGMS · UNIVERSITY OF RHODE ISLAND · PI Bongsup P Cho · 2012 to 2026
$63.6M
Regulation of the Mono-Ubiquitination of the Fanconi Anemia D2 ProteinR01HL101977 · NHLBI · UNIVERSITY OF RHODE ISLAND · PI HOWLETT, NIALL GEORGE · 2011 to 2015
$1.3M
NHLBI NIH HHS R01 HL101977NIGMS NIH HHS P20 GM103430
6 · The paper itself

Abstract

Fanconi anemia (FA) is a genetic disease characterized by bone marrow failure and increased cancer risk. The FA proteins function primarily in DNA interstrand crosslink (ICL) repair. Here, we have examined the role of the PTEN phosphatase in this process. We have established that PTEN-deficient cells, like FA cells, exhibit increased cytotoxicity, chromosome structural aberrations, and error-prone mutagenic DNA repair following exposure to ICL-inducing agents. The increased ICL sensitivity of PTEN-deficient cells is caused, in part, by elevated PLK1 kinase-mediated phosphorylation of FANCM, constitutive FANCM polyubiquitination and degradation, and the consequent inefficient assembly of the FA core complex, FANCD2, and FANCI into DNA repair foci. We also establish that PTEN function in ICL repair is dependent on its protein phosphatase activity and ability to be SUMOylated, yet is independent of its lipid phosphatase activity. Finally, via epistasis analysis, we demonstrate that PTEN and FANCD2 function cooperatively in ICL repair.

Indexed as

DNA RepairCell Cycle ProteinsCell Line, TumorChromatinChromosomal InstabilityDNA HelicasesFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsHCT116 CellsHistonesHumansMitomycinPhosphorylationPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCell Cycle ProteinsChromatinDNA HelicasesFANCD2 protein, humanFANCI protein, humanFANCM protein, humanFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsH2AX protein, humanHistonesMitomycinPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsPTEN PhosphohydrolaseRNA, Small InterferingTumor Suppressor p53-Binding Protein 1

Identifiers

PMID27819275
PMCPMC5098254
OpenAlexW2554310780

What OpenQuestion holds

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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.