Evidence map›Paper›PMID 11157988›Full record

ArticleThe Journal of cell biology2001

Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis.

F Aoudjit, K Vuori

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 284 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Regulation of anoikis by extrinsic death receptor pathways.Cell communication and signaling : CCS · 2023
    Review
  13. The Roles of Periodontal Bacteria in Atherosclerosis.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. XIAP as a multifaceted molecule in Cellular Signaling.Apoptosis : an international journal on programmed cell death · 2022
    Review
  18. Review
  19. Review
  20. Review

37 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

2 authors at 1 institution in 1 country.

F AoudjitCancer Research Center, The Burnham Institute, La Jolla, California 92037, USA.
K Vuori
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

SIGNAL TRANSDUCTION BY P130CAS AND C CRKR01CA071560 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI VUORI, KRISTIINA · 1996 to 2004
$2.0M
SIGNAL TRANSDUCTION THOUGH THE C-CBL PROTOONCOGENER01CA076037 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI VUORI, KRISTIINA · 1998 to 2001
$558k
NCI NIH HHS CA71560NCI NIH HHS CA76037NCI NIH HHS R01 CA071560
6 · The paper itself

Abstract

Survival of endothelial cells is critical for cellular processes such as angiogenesis. Cell attachment to extracellular matrix inhibits apoptosis in endothelial cells both in vitro and in vivo, but the molecular mechanisms underlying matrix-induced survival signals or detachment-induced apoptotic signals are unknown. We demonstrate here that matrix attachment is an efficient regulator of Fas-mediated apoptosis in endothelial cells. Thus, matrix attachment protects cells from Fas-induced apoptosis, whereas matrix detachment results in susceptibility to Fas-mediated cell death. Matrix attachment modulates Fas-mediated apoptosis at two different levels: by regulating the expression level of Fas, and by regulating the expression level of c-Flip, an endogenous antagonist of caspase-8. The extracellular signal-regulated kinase (Erk) cascade functions as a survival pathway in adherent cells by regulating c-Flip expression. We further show that detachment-induced cell death, or anoikis, itself results from activation of the Fas pathway by its ligand, Fas-L. Fas-L/Fas interaction, Fas-FADD complex formation, and caspase-8 activation precede the bulk of anoikis in endothelial cells, and inhibition of any of these events blocks anoikis. These studies identify matrix attachment as a survival factor against death receptor-mediated apoptosis and provide a molecular mechanism for anoikis and previously observed Fas resistance in endothelial cells.

Indexed as

Intracellular Signaling Peptides and ProteinsAnoikisApoptosisCarrier ProteinsCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Caspase 9Caspase InhibitorsCaspasesCell LineCell-Matrix JunctionsDNA FragmentationEndothelium, VascularFas Ligand Proteinfas ReceptorFlow CytometryCarrier ProteinsCASP8 and FADD-Like Apoptosis Regulating ProteinCASP8 protein, humanCASP9 protein, humanCaspase 8Caspase 9Caspase InhibitorsCaspasesCFLAR protein, humanFASLG protein, humanFas Ligand Proteinfas ReceptorIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsPhosphatidylinositol 3-KinasesRecombinant Fusion Proteins

Identifiers

PMID11157988
PMCPMC2196007
OpenAlexW2011468496

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.