Evidence map›Paper›PMID 11248093›Full record

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

The dependence receptor DCC (deleted in colorectal cancer) defines an alternative mechanism for caspase activation.

C Forcet, X Ye, L Granger, V Corset, H Shin, D E Bredesen, P Mehlen

Open access · greenAbstract 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 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
4.7field-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

86 citing papers in PubMed, 200 citations in OpenAlex.

  1. Article
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  9. Serum netrin-1 and netrin receptor levels in fibromyalgia and osteoarthritis.Turkish journal of physical medicine and rehabilitation · 2022
    Article
  10. Non-Canonical Roles of Apoptotic Caspases in the Nervous System.Frontiers in cell and developmental biology · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Netrin1 deficiency activates MST1 via UNC5B receptor, promoting dopaminergic apoptosis in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. CoalteredClinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  17. Review
  18. Article
  19. The Role of Apoptotic Signaling in Axon Guidance.Journal of developmental biology · 2018
    Review
  20. Review

26 more citing papers are in PubMed but not listed here.

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 ForcetApoptosis/Differentiation Laboratory, Molecular and Cellular Genetic Center, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5534, University of Lyon, 69622 Villeurbanne, France.
X Ye
L Granger
V Corset
H Shin
D E Bredesen
P Mehlen
Buck Institute for Research on Aging · USUniversité Claude Bernard Lyon 1 · FR

Funding

SPHINGOMYELIN SIGNALING PATHWAY IN FAS-INDUCED APOPTOSISP01CA069381 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 1996 to 2009
$16.8M
Novel apoptotic pathway activated by misfolded proteinsR01NS033376 · NINDS · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI BREDESEN, DALE E. · 1997 to 2007
$2.6M
NCI NIH HHS CA69381NCI NIH HHS P01 CA069381NINDS NIH HHS NS33376NINDS NIH HHS R01 NS033376
6 · The paper itself

Abstract

The expression of DCC (deleted in colorectal cancer) is often markedly reduced in colorectal and other cancers. However, the rarity of point mutations identified in DCC coding sequences and the lack of a tumor predisposition phenotype in DCC hemizygous mice have raised questions about its role as a tumor suppressor. DCC also mediates axon guidance and functions as a dependence receptor; such receptors create cellular states of dependence on their respective ligands by inducing apoptosis when unoccupied by ligand. We now show that DCC drives cell death independently of both the mitochondria-dependent pathway and the death receptor/caspase-8 pathway. Moreover, we demonstrate that DCC interacts with both caspase-3 and caspase-9 and drives the activation of caspase-3 through caspase-9 without a requirement for cytochrome c or Apaf-1. Hence, DCC defines an additional pathway for the apoptosome-independent caspase activation.

Indexed as

ApoptosisGenes, Tumor SuppressorCaspase 3Caspase 9CaspasesCell Adhesion MoleculesCell Line, TransformedColorectal NeoplasmsDCC ReceptorEnzyme ActivationHumansReceptors, Cell SurfaceTumor Cells, CulturedTumor Suppressor ProteinsCASP3 protein, humanCASP9 protein, humanCaspase 3Caspase 9CaspasesCell Adhesion MoleculesDCC protein, humanDCC ReceptorReceptors, Cell SurfaceTumor Suppressor Proteins

Identifiers

PMID11248093
PMCPMC30668
OpenAlexW2067759452

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.