Evidence map›Paper›PMID 15531922›Full record

ArticleOncogene2005

Type I and type II reactions in TRAIL-induced apoptosis -- results from dose-response studies.

Justine Rudner, Verena Jendrossek, Kirsten Lauber, Peter T Daniel, Sebastian Wesselborg, Claus Belka

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Tocotrienols Modulate a Life or Death Decision in Cancers.International journal of molecular sciences · 2019
    Review
  9. Article
  10. Article
  11. Onto better TRAILs for cancer treatment.Cell death and differentiation · 2016
    Review
  12. Article
  13. Article
  14. Modulation of Mcl-1 sensitizes glioblastoma to TRAIL-induced apoptosis.Apoptosis : an international journal on programmed cell death · 2014
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 2 countries.

Justine RudnerDepartment of Radiation Oncology, University of Tuebingen, Hoppe-Seyler-Str. 3, Tuebingen D-72076, Germany.
Verena Jendrossek
Kirsten Lauber
Peter T Daniel
Sebastian Wesselborg
Claus Belka
University of Tübingen · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death receptor-induced apoptosis is paradigmatically mediated via the recruitment of FADD adapter molecule to the ligand/receptor complex and subsequent activation of caspase-8. However, several observations provided evidence that components of the mitochondrial apoptosis pathway are involved in death receptor-mediated apoptosis. In this regard, caspase-8-mediated activation of Bid induces the release of cytochrome c from the mitochondria, which, in turn, triggers the formation of the apoptosome protein complex, resulting in the activation of caspase-9. Whereas Bax or Bak were shown to be required for the proapoptotic effect of Bid, Bcl-2 was described to interfere with its action. Up to now, contradictory results regarding the role of Bcl-2 in TRAIL-induced apoptosis have been published. In order to study the influence of Bcl-2 on TRAIL-induced cell death more detailed, we utilized a tetracycline-regulated Bcl-2 expression system in Jurkat T cells. After having analysed the dose response for TRAIL-induced activation of caspase-8, -9, -3, breakdown of the mitochondrial membrane potential, and changes in the apoptotic morphology in cells expressing different Bcl-2 levels, we conclude that overexpression of Bcl-2 mediates a partial resistance towards lower doses of TRAIL that can be overcome when higher doses of TRAIL are applied. Thus, the requirement of the mitochondrial pathway for death receptor-induced apoptosis in type II cells should be reconsidered, since the protective effect of Bcl-2 is limited to lower TRAIL doses or early observation time points.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsCaspasesDose-Response Relationship, DrugHumansJurkat CellsKineticsMembrane GlycoproteinsProto-Oncogene Proteins c-bcl-2Time FactorsTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alphaAntineoplastic AgentsApoptosis Regulatory ProteinsCaspasesMembrane GlycoproteinsProto-Oncogene Proteins c-bcl-2TNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID15531922
OpenAlexW2088264970

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.