Evidence map›Paper›PMID 22327219›Full record

ArticleThe EMBO journal2012

IAPs limit activation of RIP kinases by TNF receptor 1 during development.

Maryline Moulin, Holly Anderton, Anne K Voss, Tim Thomas, Wendy Wei-Lynn Wong, Aleksandra Bankovacki, Rebecca Feltham, Diep Chau, Wendy D Cook, John Silke and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
9.7field-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

121 citing papers in PubMed, 189 citations in OpenAlex.

  1. Article
  2. Mechanisms, regulation and clinical relevance of necroptosis.Nature reviews. Molecular cell biology · 2026
    Review
  3. Article
  4. Article
  5. Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026
    Review
  6. Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Death by TNF: a road to inflammation.Nature reviews. Immunology · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022
    Review
  18. Roles of RIPK3 in necroptosis, cell signaling, and disease.Experimental & molecular medicine · 2022
    Review
  19. Review
  20. XIAP as a multifaceted molecule in Cellular Signaling.Apoptosis : an international journal on programmed cell death · 2022
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Maryline MoulinLa Trobe Institute for Molecular Science, La Trobe University, Victoria, Australia.
Holly Anderton
Anne K Voss
Tim Thomas
Wendy Wei-Lynn Wong
Aleksandra Bankovacki
Rebecca Feltham
Diep Chau
Wendy D Cook
John Silke
David L Vaux
La Trobe University · AUWalter and Eliza Hall Institute of Medical Research · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibitor of apoptosis (IAP) proteins cIAP1, cIAP2, and XIAP (X-linked IAP) regulate apoptosis and cytokine receptor signalling, but their overlapping functions make it difficult to distinguish their individual roles. To do so, we deleted the genes for IAPs separately and in combination. While lack of any one of the IAPs produced no overt phenotype in mice, deletion of cIap1 with cIap2 or Xiap resulted in mid-embryonic lethality. In contrast, Xiap(-/-)cIap2(-/-) mice were viable. The death of cIap2(-/-)cIap1(-/-) double mutants was rescued to birth by deletion of tumour necrosis factor (TNF) receptor 1, but not TNFR2 genes. Remarkably, hemizygosity for receptor-interacting protein kinase 1 (Ripk1) allowed Xiap(-/-)cIap1(-/-) double mutants to survive past birth, and prolonged cIap2(-/-)cIap1(-/-) embryonic survival. Similarly, deletion of Ripk3 was able to rescue the mid-gestation defect of cIap2(-/-)cIap1(-/-) embryos, as these embryos survived to E15.5. cIAPs are therefore required during development to limit activity of RIP kinases in the TNF receptor 1 signalling pathway.

Indexed as

AnimalsFemaleGene DeletionInhibitor of Apoptosis ProteinsMaleMiceReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISignal TransductionInhibitor of Apoptosis ProteinsReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRipk1 protein, mouseRipk3 protein, mouseTnfrsf1a protein, mouse

Identifiers

PMID22327219
PMCPMC3321198
OpenAlexW1857408336

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.