Evidence map›Paper›PMID 8710904›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Constitutive overexpression of Cu/Zn superoxide dismutase exacerbates kainic acid-induced apoptosis of transgenic-Cu/Zn superoxide dismutase neurons.

O Bar-Peled, E Korkotian, M Segal, Y Groner

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-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

22 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
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  4. Review
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  10. Superoxide dismutase 1 modulates expression of transferrin receptor.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2006
    Article
  11. Induction of oxidative stress responses by dioxin and other ligands of the aryl hydrocarbon receptor.Dose-response : a publication of International Hormesis Society · 2006
    Article
  12. ets-2 promotes the activation of a mitochondrial death pathway in Down's syndrome neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  13. Article
  14. Global loss of Na,K-ATPase and its nitric oxide-mediated regulation in a transgenic mouse model of amyotrophic lateral sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  15. Article
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  19. Review
  20. Altered Ca2+ signaling and mitochondrial deficiencies in hippocampal neurons of trisomy 16 mice: a model of Down's syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    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 1 institution in 1 country.

O Bar-PeledDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
E Korkotian
M Segal
Y Groner
Weizmann Institute of Science · IL

Funding

CLONING OF HUMAN GENES INVOLVED IN DOWN'S SYNDROMER01HD021229 · NICHD · WEIZMANN INSTITUTE OF SCIENCE · PI GRONER, YORAM · 1986 to 1994
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NICHD NIH HHS HD21229
6 · The paper itself

Abstract

Cu/Zn superoxide dismutase (Cu/Zn SOD) is a key enzyme in the metabolism of oxygen free radicals. The gene resides on chromosome 21 and is overexpressed in patients with Down syndrome. Cultured neurons of transgenic Cu/Zn SOD (Tg-Cu/Zn SOD) mice with elevated activity of Cu/Zn SOD were used to determine whether constitutive overexpression of Cu/Zn SOD creates an indigenous oxidative stress that predisposes the Tg-Cu/Zn SOD neurons to added insults. Neurons from three independently derived Tg-Cu/Zn SOD strains showed higher susceptibility than nontransgenic neurons to kainic acid (KA)-mediated excitotoxicity, reflected by an earlier onset and enhanced apoptotic cell death. This higher susceptibility of transgenic neurons to KA-mediated apoptosis was associated with a chronic prooxidant state that was manifested by reduced levels of cellular glutathione and altered [Ca2+]i homeostasis. The data are compatible with the thesis that overexpression of Cu/Zn SOD creates chronic oxidative stress in the transgenic neurons, which exacerbates their susceptibility to additional insults such as KA-mediated excitotoxicity.

Indexed as

AnimalsApoptosisBrainCalciumCells, CulturedCell SurvivalDNA DamageGlutathioneKainic AcidMiceMice, TransgenicNeurogliaNeuronsOxidation-ReductionSpinal CordSuperoxide DismutaseCalciumGlutathioneKainic AcidSuperoxide Dismutase

Identifiers

PMID8710904
PMCPMC38706
OpenAlexW2039650042

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.