Evidence map›Paper›PMID 23974097›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Tumor protein D52 represents a negative regulator of ATM protein levels.

Yuyan Chen, Alvin Kamili, Jayne R Hardy, Guy E Groblewski, Kum Kum Khanna, Jennifer A Byrne

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Tumor-suppressive microRNA-34a inhibits breast cancer cell migration and invasion via targeting oncogenic TPD52.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Tumor protein D52 (TPD52) and cancer-oncogene understudy or understudied oncogene?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  12. Novel targets for ATM-deficient malignancies.Molecular & cellular oncology · 2014
    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

6 authors at 3 institutions in 2 countries.

Yuyan ChenMolecular Oncology Laboratory; Children's Cancer Research Unit; Kids Research Institute; The Children's Hospital at Westmead; Sydney, NSW Australia; The University of Sydney Discipline of Paediatrics and Child Health; The Children's Hospital at Westmead; Sydney, NSW Australia.
Alvin Kamili
Jayne R Hardy
Guy E Groblewski
Kum Kum Khanna
Jennifer A Byrne
Children's Hospital at Westmead · AUBrisbane School of Theology · AUUniversity of Wisconsin–Madison · US

Funding

Acinar Cell Biology and Pancreatic DiseaseR01DK070888 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI GROBLEWSKI, GUY E · 2006 to 2021
$4.0M
NIDDK NIH HHS R01 DK070888
6 · The paper itself

Abstract

Tumor protein D52 (TPD52) is a coiled-coil motif bearing hydrophilic polypeptide known to be overexpressed in cancers of diverse cellular origins. Increased TPD52 expression is associated with increased proliferation and invasive capacity in different cell types. Recent studies have reported a correlation between TPD52 transcript levels and G 2 chromosomal radiosensitivity in lymphocytes of women at risk of hereditary breast cancer, and that TPD52 knockdown significantly reduced the radiation sensitivity of multiple cancer cell lines. In this study, we investigated possible roles for TPD52 in DNA damage response, and found that increased TPD52 expression in breast cancer and TPD52-expressing BALB/c 3T3 cells compromised ATM-mediated cellular responses to DNA double-strand breaks induced by γ-ray irradiation, which was associated with downregulation of steady-state ATM protein, but not transcript levels, regardless of irradiation status. TPD52-expressing 3T3 cells also showed significantly increased radiation sensitivity compared with vector cells evaluated by clonogenic assays. Furthermore, direct interactions between exogenous and endogenous ATM and TPD52 were detected by GST pull-down and co-immunoprecipitation assays. We also identified the interaction domains involved in this binding as TPD52 residues 111-131, and ATM residues 1-245 and 772-1102. Taken together, our results suggest that TPD52 may represent a novel negative regulator of ATM protein levels.

Indexed as

3T3 CellsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorDNA Breaks, Double-StrandedDNA RepairDown-RegulationGamma RaysHistonesHumansMCF-7 CellsMiceNeoplasm ProteinsProtein BindingRNA InterferenceRNA, Small InterferingAtaxia Telangiectasia Mutated ProteinsH2AX protein, humanHistonesNeoplasm ProteinsRNA, Small InterferingTPD52 protein, humanATMcancerDNA damage responseprotein-protein interactionTPD52

Identifiers

PMID23974097
PMCPMC3875682
OpenAlexW2023445541

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.