Evidence map›Paper›PMID 31560400›Full record

ArticleMolecular biology and evolution2020

Tolerance to Selenoprotein Loss Differs between Human and Mouse.

Didac Santesmasses, Marco Mariotti, Vadim N Gladyshev

Open access · bronzeAbstract read
In one paragraph

Article in Molecular biology and evolution, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. SELENOI Functions as a Key Modulator of Ferroptosis Pathway in Colitis and Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Selenoprotein S: A versatile disordered protein.Archives of biochemistry and biophysics · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Didac SantesmassesDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Marco MariottiDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Vadim N GladyshevDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Brigham and Women's Hospital · US

Funding

Methionine sulfoxide reduction, selenium and agingR01AG021518 · NIA · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2003 to 2018
$5.0M
Selenoproteins as Targets for Cancer PreventionR01CA080946 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2001 to 2018
$4.5M
Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
Systems level understanding of selenoprotein biosynthesisR01DK117149 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2018 to 2022
$2.4M
NCI NIH HHS R01 CA080946NIA NIH HHS R01 AG021518NIDDK NIH HHS R01 DK117149NIGMS NIH HHS R37 GM065204
6 · The paper itself

Abstract

Mouse has emerged as the most common model organism in biomedicine. Here, we analyzed the tolerance to the loss-of-function (LoF) of selenoprotein genes, estimated from mouse knockouts and the frequency of LoF variants in humans. We found not only a general correspondence in tolerance (e.g., GPX1, GPX2) and intolerance (TXNRD1, SELENOT) to gene LoF between humans and mice but also important differences. Notably, humans are intolerant to the loss of iodothyronine deiodinases, whereas their deletion in mice leads to mild phenotypes, and this is consistent with phenotype differences in selenocysteine machinery loss between these species. In contrast, loss of TXNRD2 and GPX4 is lethal in mice but may be tolerated in humans. We further identified the first human SELENOP variants coding for proteins varying in selenocysteine content. Finally, our analyses suggested that premature termination codons in selenoprotein genes trigger nonsense-mediated decay, but do this inefficiently when UGA codon is gained. Overall, our study highlights differences in the physiological importance of selenoproteins between human and mouse.

Indexed as

Loss of Function MutationAnimalsGene Knockout TechniquesHumansMiceNonsense Mediated mRNA DecayPhenotypeRNA, MessengerSelenoproteinsSpecies SpecificityRNA, MessengerSelenoproteinshumanknockoutmousemutationselenocysteineselenoprotein

Identifiers

PMID31560400
PMCPMC6993852
OpenAlexW2976765201

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.