Evidence map›Paper›PMID 25336634›Full record

ArticleThe Journal of biological chemistry2014

Selenoprotein H suppresses cellular senescence through genome maintenance and redox regulation.

Ryan T Y Wu, Lei Cao, Benjamin P C Chen, Wen-Hsing Cheng

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Effects of selenoprotein extracts fromFrontiers in immunology · 2024
    Article
  11. Article
  12. Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  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 2 institutions in 1 country.

Ryan T Y WuFrom the Department of Nutrition and Food Science, University of Maryland, College Park, Maryland 20742.
Lei CaoDepartment of Food Science, Nutrition, and Health Promotion, Mississippi State University, Mississippi State, Mississippi 39762, and.
Benjamin P C ChenDivision of Molecular Radiation Biology, Department of Radiation Oncology, Southwestern Medical Center at Dallas, University of Texas, Dallas, Texas 75390.
Wen-Hsing ChengFrom the Department of Nutrition and Food Science, University of Maryland, College Park, Maryland 20742, Department of Food Science, Nutrition, and Health Promotion, Mississippi State University, Mississippi State, Mississippi 39762, and wc523@msstate.edu.
University of Maryland, College Park · USThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and persistent DNA damage response contribute to cellular senescence, a degeneration process critically involving ataxia telangiectasia-mutated (ATM) and p53. Selenoprotein H (SelH), a nuclear selenoprotein, is proposed to carry redox and transactivation domains. To determine the role of SelH in genome maintenance, shRNA knockdown was employed in human normal and immortalized cell lines. SelH shRNA MRC-5 diploid fibroblasts under ambient O2 displayed a distinct profile of senescence including β-galactosidase expression, autofluorescence, growth inhibition, and ATM pathway activation. Such senescence phenotypes were alleviated in the presence of ATM kinase inhibitors, by p53 shRNA knockdown, or by maintaining the cells under 3% O2. During the course of 5-day recovery, the induction of phospho-ATM on Ser-1981 and γH2AX by H2O2 treatment (20 μm) subsided in scrambled shRNA but exacerbated in SelH shRNA MRC-5 cells. Results from clonogenic assays demonstrated hypersensitivity of SelH shRNA HeLa cells to paraquat and H2O2, but not to hydroxyurea, neocarzinostatin, or camptothecin. While SelH mRNA expression was induced by H2O2 treatment, SelH-GFP did not mobilize to sites of oxidative DNA damage. The glutathione level was lower in SelH shRNA than scrambled shRNA HeLa cells, and the H2O2-induced cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor. Altogether, SelH protects against cellular senescence to oxidative stress through a genome maintenance pathway involving ATM and p53.

Indexed as

Genome, HumanAcetylcysteineAtaxia Telangiectasia Mutated Proteinsbeta-GalactosidaseCell LineCellular SenescenceDNA-Binding ProteinsFibroblastsGene Expression RegulationGenomic InstabilityHeLa CellsHumansHydrogen PeroxideOxidation-ReductionOxidative StressParaquatAcetylcysteineAtaxia Telangiectasia Mutated ProteinsATM protein, humanbeta-GalactosidaseDNA-Binding ProteinsHydrogen PeroxideParaquatProtein Kinase InhibitorsRecombinant Fusion ProteinsRNA, Small Interferingselenoprotein H, humanSelenoproteinsTumor Suppressor Protein p53Ataxia Telangiectasiap53Reactive Oxygen Species (ROS)SeleniumSenescence

Identifiers

PMID25336634
PMCPMC4256366
OpenAlexW2004828905

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.