Evidence map›Paper›PMID 22332043›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2011

Selenium regulation of the selenoprotein and nonselenoprotein transcriptomes in rodents.

Roger A Sunde, Anna M Raines

Open access · greenAbstract readReview
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

79 citing papers in PubMed, 184 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Mitochondrial Reactive Oxygen Species (mROS) Generation and Cancer:International journal of nanomedicine · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. "Alphabet" Selenoproteins: Implications in Pathology.International journal of molecular sciences · 2023
    Review
  15. α-lipoic acid ameliorates consequences of copper overload by up-regulating selenoproteins and decreasing redox misbalance.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Selenium status and type 2 diabetes risk.Archives of biochemistry and biophysics · 2022
    Review
  18. Review
  19. Review
  20. Article

19 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Roger A SundeDepartment of Nutritional Sciences, University of Wisconsin, Madison, WI 53706, USA. sunde@nutrisci.wisc.edu.
Anna M Raines
University of Wisconsin–Madison · US

Funding

TRAINING IN NUTRITIONT32DK007665 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI GUY E GROBLEWSKI, Chi- Liang Eric Yen · 1993 to 2026
$9.2M
Development of molecular biology-based assays for human selenium statusR01DK074184 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI SUNDE, ROGER A · 2006 to 2007
$351k
NIDDK NIH HHS NIH DK74184NIDDK NIH HHS R01 DK074184NIDDK NIH HHS T32 DK007665NIDDK NIH HHS T32-DK07665
6 · The paper itself

Abstract

This review discusses progress in understanding the hierarchy of selenoprotein expression at the transcriptome level from selenium (Se) deficiency to Se toxicity. Microarray studies of the full selenoproteome have found that 5 of 24 rodent selenoprotein mRNA decrease to <40% of Se adequate levels in Se deficient liver but that the majority of selenoprotein mRNA are not regulated by Se deficiency. These differences match with the hierarchy of selenoprotein expression, helping to explain these differences and also showing that selenoprotein transcripts can be used as molecular biomarkers for assessing Se status. The similarity of the response curves for regulated selenoproteins suggests one underlying mechanism is responsible for the downregulation of selenoprotein mRNA in Se deficiency, but the heterogeneity of the UGA position in regulated and nonregulated selenoprotein transcripts now indicates that current nonsense mediated decay models cannot explain which transcripts are susceptible to mRNA decay. Microarray studies on the full liver transcriptome in rats found only <10 transcripts/treatment were significantly down- or upregulated by Se deficiency or by supernutritional Se up to 2.0 μg Se/g diet (20× requirement), suggesting that cancer prevention associated with supernutritional Se may not be mediated by transcriptional changes. Toxic dietary Se at 50× requirement (5 μg Se/g diet), however, significantly altered ∼4% of the transcriptome, suggesting number of transcriptional changes itself as a biomarker of Se toxicity. Finally, panels of Se regulated selenoprotein plus nonselenoprotein transcripts predict Se status from deficient to toxic better than conventional biomarkers, illustrating potential roles for molecular biomarkers in nutrition.

Indexed as

AnimalsDietFemaleLiverMaleMicroarray AnalysisNutritional StatusRatsRNA, MessengerSeleniumSelenoproteinsTranscriptomeRNA, MessengerSeleniumSelenoproteins

Identifiers

PMID22332043
PMCPMC3065762
OpenAlexW2153424390

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.