Evidence map›Paper›PMID 11549720›Full record

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

Caspases 3 and 9 send a pro-apoptotic signal from synapse to cell body in olfactory receptor neurons.

C M Cowan, J Thai, S Krajewski, J C Reed, D W Nicholson, S H Kaufmann, A J Roskams

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
3.7field-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

46 citing papers in PubMed, 134 citations in OpenAlex.

  1. BlackenedMolecules (Basel, Switzerland) · 2026
    Article
  2. Article
  3. The concealed side of caspases: beyond a killer of cells.Cellular and molecular life sciences : CMLS · 2024
    Review
  4. Article
  5. Marine-derived Compounds: A Powerful Platform for the Treatment of Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Prion protein and aging.Frontiers in cell and developmental biology · 2014
    Review
  19. Article
  20. A caspase cascade regulating developmental axon degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

7 authors at 2 institutions in 2 countries.

C M CowanCentre for Molecular Medicine and Therapeutics, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
J Thai
S Krajewski
J C Reed
D W Nicholson
S H Kaufmann
A J Roskams
University of British Columbia · CASanford Burnham Prebys Medical Discovery Institute · US

Funding

Role of Proteases in Therapy-Induced ApoptosisR01CA069008 · NCI · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H · 1995 to 2010
$3.4M
Caspases, Calpains and Neuronal Cell deathR01NS036821 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI KRAJEWSKI, STAN · 1999 to 2006
$2.9M
NCI NIH HHS R01 CA069008NINDS NIH HHS NS36821NINDS NIH HHS R01 NS036821
6 · The paper itself

Abstract

Caspase-9, an initiator caspase, and caspase-3, an effector caspase, have been suggested to mediate the terminal stages of neuronal apoptosis, but little is known about their activation in vivo. We examined temporal and spatial aspects of caspase-9 and -3 activation in olfactory receptor neurons (ORNs) undergoing apoptosis after target removal in vivo. After removal of the olfactory bulb, enhanced expression of procaspase-9 and -3 is observed in ORNs, followed by activation initially at the level of the lesion, then in axons, and only later in the ORN soma. We established the amyloid precursor-like protein-2 (APLP2) as a caspase substrate that is cleaved in an identical spatiotemporal pattern, suggesting its cleavage is the result of retrograde propagation of a pro-apoptotic signal in a caudorostral wave from the synapse through the axon to the ORN cell body. A null mutation in caspase-3 causes a change in axonal patterning indicative of an overall developmental expansion of the ORN population, and mature ORNs of caspase-3 knock-outs do not undergo caspase-dependent terminal dUTP nick end labeling-positive apoptosis after olfactory bulb removal. These results demonstrate that ORNs require caspase-3 activation to undergo normal developmental and mature target-deprived apoptosis. In addition, we demonstrate an axonal site of action for caspase-3 and -9 and show that regulation and activation of caspase-3 and -9 leading to apoptosis is a highly ordered process that occurs initially at the presynaptic level and only later at the cell body after deafferentation.

Indexed as

Amyloid beta-Protein PrecursorAnimalsApoptosisAxonsCaspase 3Caspase 9CaspasesEnzyme ActivationImmunohistochemistryIn Situ Nick-End LabelingMiceMice, KnockoutNerve Tissue ProteinsOlfactory Receptor NeuronsSignal TransductionSynapsesAmyloid beta-Protein PrecursorAPLP1 protein, humanAplp1 protein, mouseAplp2 protein, mouseCASP3 protein, humanCasp3 protein, mouseCASP9 protein, humanCasp9 protein, mouseCaspase 3Caspase 9CaspasesNerve Tissue Proteins

Identifiers

PMID11549720
PMCPMC6763014
OpenAlexW1912063668

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.