Evidence map›Paper›PMID 24974905›Full record

ReviewBiological trace element research2014

Selenoproteins in nervous system development and function.

Matthew W Pitts, China N Byrns, Ashley N Ogawa-Wong, Penny Kremer, Marla J Berry

Open access · greenAbstract readReview
In one paragraph

Review in Biological trace element research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Ferroptosis and Pyroptosis in Epilepsy.Molecular neurobiology · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Trace Element Selenium Effectively Alleviates Intestinal Diseases.International journal of molecular sciences · 2021
    Review
  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

5 authors at 2 institutions in 1 country.

Matthew W PittsDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, 651 Ilalo St, Honolulu, HI, 96813, USA, mwpitts@hawaii.edu.
China N Byrns
Ashley N Ogawa-Wong
Penny Kremer
Marla J Berry
University of Hawaiʻi at Mānoa · USUniversity of Hawaii System · US

Funding

WORLDWIDE EPIDEMIOLOGY &EPIZOOTIOLOGY OF HANTAVIRUSG12RR003061 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI COUVILLON, PATRICIA A · 1986 to 2011
$32.3M
RESEARCH DESIGN, BIOSTATISTICS AND RESEARCH ETHICS COREG12MD007601 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 2012 to 2016
$13.0M
MECHANISM OF SELENOPROTEIN SYNTHESIS IN EUKARYOTESR01DK047320 · NIDDK · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 1994 to 2020
$5.8M
NCRR NIH HHS G12 RR003061NIDDK NIH HHS R01 DK047320NIMHD NIH HHS G12 MD007601
6 · The paper itself

Abstract

Selenoproteins are a distinct class of proteins that are characterized by the co-translational incorporation of selenium (Se) in the form of the 21st amino acid selenocysteine. Selenoproteins provide a key defense against oxidative stress, as many of these proteins participate in oxidation-reduction reactions neutralizing reactive oxygen species, where selenocysteine residues act as catalytic sites. Many selenoproteins are highly expressed in the brain, and mouse knockout studies have determined that several are required for normal brain development. In parallel with these laboratory studies, recent reports of rare human cases with mutations in genes involved in selenoprotein biosynthesis have described individuals with an assortment of neurological problems that mirror those detailed in knockout mice. These deficits include impairments in cognition and motor function, seizures, hearing loss, and altered thyroid metabolism. Additionally, due to the fact that oxidative stress is a key feature of neurodegenerative disease, there is considerable interest in the therapeutic potential of selenium supplementation for human neurological disorders. Studies performed in cell culture and rodent models have demonstrated that selenium administration attenuates oxidative stress, prevents neurodegeneration, and counters cell signaling mechanisms known to be dysregulated in certain disease states. However, there is currently no definitive evidence in support of selenium supplementation to prevent and/or treat common neurological conditions in the general population. It appears likely that, in humans, supplementation with selenium may only benefit certain subpopulations, such as those that are either selenium-deficient or possess genetic variants that affect selenium metabolism.

Indexed as

AnimalsBrainHumansMice, KnockoutMutationNervous System DiseasesOrganogenesisOxidative StressSelenoproteinsSelenoproteins

Identifiers

PMID24974905
PMCPMC4222985
OpenAlexW2002289370

What OpenQuestion holds

Textmetadata
LicenceTDM
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.