Evidence map›Paper›PMID 11312276›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

How protein kinase C activation protects nerve cells from oxidative stress-induced cell death.

P Maher

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.6field-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

46 citing papers in PubMed, 214 citations in OpenAlex.

  1. Review
  2. Article
  3. Nanomedicine: A New Frontier in Alzheimer's Disease Drug Targeting.Central nervous system agents in medicinal chemistry · 2025
    Review
  4. Review
  5. Article
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  8. Article
  9. Neuroprotective Properties of Green Tea (Molecules (Basel, Switzerland) · 2020
    Review
  10. Article
  11. Article
  12. BioMed research international · 2019
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. PKC in developmental hypothyroid rat brain.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Review
  18. Lead exposure disrupts global DNA methylation in human embryonic stem cells and alters their neuronal differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

P MaherDepartment of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, USA. pmaher@scripps.edu
Scripps Research Institute · US

Funding

STROKE THERAPY MECHANISMS WITH NEUROTROPHIC FACTORSP01NS028121 · NINDS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI ZIVIN, JUSTIN A. · 1990 to 2004
$6.4M
NINDS NIH HHS NS28121NINDS NIH HHS P01 NS028121
6 · The paper itself

Abstract

Oxidative stress is implicated in the nerve cell death that occurs in a variety of neurological disorders, and the loss of protein kinase C (PKC) activity has been coupled to the severity of the damage. The functional relationship between stress, PKC, and cell death is, however, unknown. Using an immortalized hippocampal cell line that is particularly sensitive to oxidative stress, I show that activation of PKC by the phorbol ester tetradecanoylphorbol acetate (TPA) inhibits cell death via the stimulation of a complex protein phosphorylation pathway. TPA treatment leads to the rapid activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), the inactivation of p38 mitogen-activated protein kinase (MAPK), and the downregulation of PKCdelta. Inhibition of either ERK or JNK activation blocks TPA-mediated protection, whereas p38 MAPK and PKCdelta inhibitors block stress-induced nerve cell death. Both p38 MAPK inactivation and JNK activation appear to be downstream of ERK because an agent that blocks ERK activation also blocks the modulation of these other MAP kinase family members by TPA treatment. Thus, the protection from oxidative stress afforded nerve cells by PKC activity requires the combined modulation of multiple enzyme pathways and suggests why the loss of PKC activity contributes to nerve cell death.

Indexed as

AnimalsButhionine SulfoximineCalcium-Calmodulin-Dependent Protein KinasesCell CountCell DeathCells, CulturedCell SurvivalEnzyme ActivationEnzyme InhibitorsFlavonoidsGlutamic AcidHomocysteineIsoenzymesMiceMitogen-Activated Protein KinasesNeurons2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneButhionine SulfoximineCalcium-Calmodulin-Dependent Protein KinasesEnzyme InhibitorsFlavonoidsGlutamic Acidhomocysteic acidHomocysteineIsoenzymesMitogen-Activated Protein KinasesPhosphotransferases (Alcohol Group Acceptor)Protein Kinase CReactive Oxygen SpeciesSphingosine KinaseTetradecanoylphorbol Acetate

Identifiers

PMID11312276
PMCPMC6762555
OpenAlexW1486333767

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.