Evidence map›Paper›PMID 19830835›Full record

ArticleJournal of neuroscience research2010

Fas activation increases neural progenitor cell survival.

Julia C Knight, Eugene L Scharf, Yang Mao-Draayer

Abstract read
In one paragraph

Article in Journal of neuroscience research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Cross-talk between CD4+ T-cells and neural stem/progenitor cells.Journal of the neurological sciences · 2011
    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

3 authors at 1 institution in 1 country.

Julia C KnightNeuroscience Graduate Program, University of Vermont, Burlington, Vermont, USA.
Eugene L Scharf
Yang Mao-Draayer
University of Vermont · US

Funding

Proteomics Core for Neuroscience P20 RR16435P20RR016435 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MARTIN-CARABALLO, MIGUEL · 2001 to 2010
$23.5M
Center for Neuroscience ExcellenceP30GM103498 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2012 to 2015
$4.3M
NCRR NIH HHS P20 RR016435NCRR NIH HHS P20 RR16435NIGMS NIH HHS P30 GM103498
6 · The paper itself

Abstract

Although there is a sizable amount of research focusing on adult neural progenitor cells (NPCs) as a therapeutic approach for many neurodegenerative diseases, including multiple sclerosis, little is known about the pathways that govern NPC survival and apoptosis. Fas, a member of the death receptor superfamily, plays a well-characterized role in the immune system, but its function in neural stem cells remains uncertain. Our study focuses on the effects of Fas on NPC survival in vitro. Activation of Fas by recombinant Fas ligand (FasL) did not induce apoptosis in murine NPCs in culture. In fact, both an increase in the amount of viable cells and a decrease in apoptotic and dying cells were observed with FasL treatment. Our data indicate that FasL-mediated adult NPC neuroprotection is characterized by a reduction in apoptosis, but not increased proliferation. Further investigation of this effect revealed that the antiapoptotic effects of FasL are mediated by the up-regulation of Birc3, an inhibitor of apoptosis protein (IAP). Conversely, the observed effect is not the result of altered caspase activation or FLIP (Fas-associated death domain-like interleukin-1beta-converting enzyme inhibitory protein) up-regulation, which is known to inhibit caspase-8-mediated cell death in T cells. Our data indicate that murine adult NPCs are resistant to FasL-induced cell death. Activation of Fas increased cell survival by decreasing apoptosis through Birc3 up-regulation. These results describe a novel pathway involved in NPC survival.

Indexed as

AnimalsAnimals, NewbornBaculoviral IAP Repeat-Containing 3 ProteinBrainBromodeoxyuridineCell ProliferationCells, CulturedCell SurvivalFas Ligand Proteinfas ReceptorFibroblast Growth FactorsFlow CytometryInhibitor of Apoptosis ProteinsIn Situ Nick-End LabelingMiceMice, Inbred C57BLBaculoviral IAP Repeat-Containing 3 ProteinBirc3 protein, mouseBromodeoxyuridineFas Ligand ProteinFas protein, mousefas ReceptorFibroblast Growth FactorsInhibitor of Apoptosis ProteinsUbiquitin-Protein Ligases

Identifiers

PMID19830835
PMCPMC4476376
OpenAlexW2043268652

What OpenQuestion holds

Textmetadata
LicenceTDM
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.