Evidence map›Paper›PMID 11134519›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Cerebellar neurons lacking complex gangliosides degenerate in the presence of depolarizing levels of potassium.

G Wu, X Xie, Z H Lu, R W Ledeen

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

35 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Review
  3. Emerging phagocytosis checkpoints in cancer immunotherapy.Signal transduction and targeted therapy · 2023
    Review
  4. Gangliosides in Neurodegenerative Diseases.Advances in neurobiology · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Nuclear sphingolipid metabolism.Annual review of physiology · 2012
    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

4 authors at 2 institutions in 1 country.

G WuDepartment of Neurosciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.
X Xie
Z H Lu
R W Ledeen
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Role of Nuclear Gangliosides in Neuronal FunctionR01NS033912 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI LEDEEN, ROBERT W · 1996 to 2012
$3.8M
NINDS NIH HHS NS33912NINDS NIH HHS R01 NS033912
6 · The paper itself

Abstract

Mice engineered to lack GM2/GD2 synthase (GalNAc-T), with resultant deficit of GM2, GD2, and all gangliotetraose gangliosides, were originally described as showing a relatively normal phenotype with only a slight reduction in nerve conduction. However, a subsequent study showed that similar animals suffer axonal degeneration, myelination defects, and impaired motor coordination. We have examined the behavior of cerebellar granule neurons from these neonatal knockouts in culture and have found evidence of impaired capacity for Ca2+ regulation. These cells showed relatively normal behavior when grown in the presence of physiological or moderately elevated K+ but gradually degenerated in the presence of high K+. This degeneration in depolarizing medium was accompanied by progressive elevation of intracellular calcium and onset of apoptosis, phenomena not observed with normal cells. No differences were detected in cells from normal vs. heterozygous mice. These findings suggest that neurons from GalNAc-T knockout mice are lacking a calcium regulatory mechanism that is modulated by one or more of the deleted gangliosides, and they support the hypothesis that maintenance of calcium homeostasis is one function of complex gangliosides during, and perhaps subsequent to, neuronal development.

Indexed as

Gene DeletionAnimalsApoptosisCalciumCell CountCells, CulturedCerebellumChromatography, Thin LayerGangliosidesGenotypeMiceMice, Inbred C57BLMice, KnockoutN-AcetylgalactosaminyltransferasesNeuronsPotassiumCalciumGangliosidesN-Acetylgalactosaminyltransferases(N-acetylneuraminyl)-galactosylglucosylceramide N-acetylgalactosaminyltransferasePotassium

Identifiers

PMID11134519
PMCPMC14586
OpenAlexW2128206096

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.