Evidence map›Paper›PMID 21959933›Full record

ReviewCell death and differentiation2012

Fas death receptor signalling: roles of Bid and XIAP.

T Kaufmann, A Strasser, P J Jost

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed
12.1field-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

186 citing papers in PubMed, 370 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Biomedical reports · 2025
    Article
  11. Article
  12. Article
  13. The critical role of X-linked inhibitor of apoptosis protein (XIAP) in tumor development.Apoptosis : an international journal on programmed cell death · 2025
    Review
  14. Article
  15. FTO controls CD8Cell death & disease · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Pharmacological targeting of caspase-8/c-FLIPCommunications biology · 2025
    Article
  20. AcetylatedFrontiers in oncology · 2025
    Article

126 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

3 authors at 3 institutions in 3 countries.

T KaufmannInstitute of Pharmacology, University of Bern, Bern, Switzerland. thomas.kaufmann@pki.unibe.ch
A Strasser
P J Jost
Klinikum rechts der Isar · DEUniversity of Bern · CHWalter and Eliza Hall Institute of Medical Research · AU

Funding

ONCOGENE-INDUCED LEUKEMOGENESIS IN TRANSGENIC MICER01CA043540 · NCI · WALTER AND ELIZA HALL INST MEDICAL RES · PI CORY, SUZANNE · 1987 to 2009
$1.7M
NCI NIH HHS CA 043540NCI NIH HHS R01 CA043540
6 · The paper itself

Abstract

Fas (also called CD95 or APO-1), a member of a subgroup of the tumour necrosis factor receptor superfamily that contain an intracellular death domain, can initiate apoptosis signalling and has a critical role in the regulation of the immune system. Fas-induced apoptosis requires recruitment and activation of the initiator caspase, caspase-8 (in humans also caspase-10), within the death-inducing signalling complex. In so-called type 1 cells, proteolytic activation of effector caspases (-3 and -7) by caspase-8 suffices for efficient apoptosis induction. In so-called type 2 cells, however, killing requires amplification of the caspase cascade. This can be achieved through caspase-8-mediated proteolytic activation of the pro-apoptotic Bcl-2 homology domain (BH)3-only protein BH3-interacting domain death agonist (Bid), which then causes mitochondrial outer membrane permeabilisation. This in turn leads to mitochondrial release of apoptogenic proteins, such as cytochrome c and, pertinent for Fas death receptor (DR)-induced apoptosis, Smac/DIABLO (second mitochondria-derived activator of caspase/direct IAP binding protein with low Pi), an antagonist of X-linked inhibitor of apoptosis (XIAP), which imposes a brake on effector caspases. In this review, written in honour of Juerg Tschopp who contributed so much to research on cell death and immunology, we discuss the functions of Bid and XIAP in the control of Fas DR-induced apoptosis signalling, and we speculate on how this knowledge could be exploited to develop novel regimes for treatment of cancer.

Indexed as

AnimalsApoptosisBH3 Interacting Domain Death Agonist ProteinCaspase 8Cell Membrane PermeabilityClinical Trials as Topicfas ReceptorHumansInhibitor of Apoptosis ProteinsMitochondriaNeoplasmsReceptors, Death DomainSignal TransductionX-Linked Inhibitor of Apoptosis ProteinBH3 Interacting Domain Death Agonist ProteinBID protein, humanCaspase 8FAS protein, humanfas ReceptorInhibitor of Apoptosis ProteinsReceptors, Death DomainX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID21959933
PMCPMC3252833
OpenAlexW2020547407

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.