Evidence map›Paper›PMID 24047694›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Chromatin PTEN is involved in DNA damage response partly through regulating Rad52 sumoylation.

Byeong Hyeok Choi, Yan Chen, Wei Dai

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. PTEN as a Guardian of the Genome: Pathways and Targets.Cold Spring Harbor perspectives in medicine · 2020
    Review
  9. PTEN Nuclear Functions.Cold Spring Harbor perspectives in medicine · 2020
    Review
  10. The nuclear phosphoinositide response to stress.Cell cycle (Georgetown, Tex.) · 2020
    Review
  11. Cancers · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Niraparib in ovarian cancer: results to date and clinical potential.Therapeutic advances in medical oncology · 2017
    Review
  18. Cell Cycle Control by PTEN.Journal of molecular biology · 2017
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Byeong Hyeok ChoiDepartments of Environmental Medicine, Biochemistry, and Molecular Pharmacology; New York University School of Medicine; Tuxedo, NY USA.
Yan Chen
Wei Dai
New York University · USUniversidad del Noreste · MXUniversity School · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 1985 to 2020
$26.1M
Molecular mechanisms underlying chromosomal instability and aneuploidyR01CA090658 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAI, WEI · 2001 to 2012
$2.9M
Study of Ras-Mediated ApoptosisR01CA100498 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2004 to 2017
$2.5M
Plk3, A New Player In The Hypoxia Regulatory Networ.R01CA150512 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAI, WEI · 2011 to 2015
$1.6M
Study of Anti-Survival signals in NF1R01CA153354 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2012 to 2017
$1.6M
Plk3 in lung cancerR03ES019929 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI XU, DAZHONG · 2011 to 2012
$160k
NCI NIH HHS CA090658NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA090658NCI NIH HHS R01 CA100498NCI NIH HHS R01 CA150512NCI NIH HHS R01 CA153354NIEHS NIH HHS ES000260NIEHS NIH HHS ES019929NIEHS NIH HHS P30 ES000260NIEHS NIH HHS R03 ES019929
6 · The paper itself

Abstract

A pool of PTEN localizes to the nucleus. However, the exact mechanism of action of nuclear PTEN remains poorly understood. We have investigated PTEN's role during DNA damage response. Here we report that PTEN undergoes chromatin translocation after DNA damage, and that its translocation is closely associated with its phosphorylation on S366/T370 but not on S380. Deletional analysis reveals that the C2 domain of PTEN is responsible for its nuclear translocation after exposure to genotoxin. Both casein kinase 2 and GSK3β are involved in the phosphorylation of the S366/T370 epitope, as well as PTEN's association with chromatin after DNA damage. Significantly, PTEN specifically interacts with Rad52 and colocalizes with Rad52, as well as γH2AX, after genotoxic stress. Moreover, PTEN is involved in regulating Rad52 sumoylation. Combined, our studies strongly suggest that nuclear/chromatin PTEN mediates DNA damage repair through interacting with and modulating the activity of Rad52.

Indexed as

DNA RepairActive Transport, Cell NucleusCasein Kinase IICell NucleusChromatinCytoplasmDNA DamageGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHeLa CellsHistonesHumansHydrogen PeroxidePhosphorylationCasein Kinase IIChromatinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanH2AX protein, humanHistonesHydrogen PeroxidePTEN PhosphohydrolasePTEN protein, humanRad52 DNA Repair and Recombination ProteinRAD52 protein, humanSerineThreoninechromatinDNA damagegenotoxic stressphosphorylationPTENRad52

Identifiers

PMID24047694
PMCPMC3895432
OpenAlexW1996648100

What OpenQuestion holds

Textmetadata
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.