Evidence map›Paper›PMID 24787014›Full record

ArticleCell death & disease2014

Nerve growth factor-mediated inhibition of apoptosis post-caspase activation is due to removal of active caspase-3 in a lysosome-dependent manner.

K Mnich, L A Carleton, E T Kavanagh, K M Doyle, A Samali, A M Gorman

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  5. Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
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  12. Zinc in the Brain: Friend or Foe?International journal of molecular sciences · 2020
    Review
  13. Review
  14. Article
  15. Nerve Growth Factor Protects Against Pyrethroid-Induced Endoplasmic Reticulum (ER) Stress in Primary Hippocampal Neurons.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  16. Article
  17. Article
  18. 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

6 authors at 2 institutions in 1 country.

K Mnich1] Apoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland [2] Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
L A CarletonApoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland.
E T KavanaghApoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland.
K M DoyleSchool of Medicine, National University of Ireland, Galway, Ireland.
A SamaliApoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland.ORCID 0000000286108375
A M GormanApoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, Ireland.
Ollscoil na Gaillimhe – University of Galway · IENational University of Ireland · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nerve growth factor (NGF) is well characterised as an important pro-survival factor in neuronal cells that can inhibit apoptotic cell death upstream of mitochondrial outer membrane permeabilisation. Here we addressed the question of whether NGF can also protect against apoptosis downstream of caspase activation. NGF treatment promoted a rapid reduction in the level of the p17 subunit of active caspase-3 in PC12 cells that had been induced to undergo apoptosis by various cytotoxins. The mechanism involved TrkA-dependent activation of extracellular signal-regulated kinase (ERK1/2) but not phosphatidylinositol 3-kinase (PI3K)/Akt, and de novo protein synthesis. Involvement of inhibitor of apoptosis proteins (IAPs) and proteasomal degradation were ruled out. In contrast, inhibition of lysosome function using chloroquine and concanamycin A reversed NGF-induced removal of p17. Moreover, in NGF-treated cells, active caspases were found to be localised to lysosomes. The involvement of macroautophagy and chaperone-mediated autophagy were ruled out. Taken together, these findings suggest an anti-apoptotic mechanism by which NGF induces removal of active caspase-3 in a lysosome-dependent manner.

Indexed as

AnimalsApoptosisAutophagyBiocatalysisCaspase 3Cell SurvivalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesKineticsLysosomesMiceMolecular ChaperonesNerve Growth FactorNeurograninPC12 CellsProteasome Endopeptidase ComplexCaspase 3Extracellular Signal-Regulated MAP KinasesMolecular ChaperonesNerve Growth FactorNeurograninProteasome Endopeptidase ComplexReceptor, trkAThapsigargin

Identifiers

PMID24787014
PMCPMC4047888
OpenAlexW1983649388

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.