Evidence map›Paper›PMID 27056574›Full record

ReviewCellular and molecular life sciences : CMLS2016

Developmental checkpoints guarded by regulated necrosis.

Christopher P Dillon, Bart Tummers, Katherine Baran, Douglas R Green

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. The potential role of necroptosis in clinical diseases (Review).International journal of molecular medicine · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Cell Death in the Kidney.International journal of molecular sciences · 2019
    Review
  9. Review
  10. Review
  11. Review
  12. Caspase-8: regulating life and death.Immunological reviews · 2017
    Review
  13. Review
  14. Review
  15. Review
  16. 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

4 authors.

Christopher P DillonDepartment of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.
Bart TummersDepartment of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.
Katherine BaranDepartment of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA. douglas.green@stjude.org.

Funding

Survival Function of the Fadd-Caspase-8-Flip Complex - MERIT ExtensionR37AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2017 to 2026
$4.5M
NIAID NIH HHS R37 AI044828
6 · The paper itself

Abstract

The process of embryonic development is highly regulated through the symbiotic control of differentiation and programmed cell death pathways, which together sculpt tissues and organs. The importance of programmed necrotic (RIPK-dependent necroptosis) cell death during development has recently been recognized as important and has largely been characterized using genetically engineered animals. Suppression of necroptosis appears to be essential for murine development and occurs at three distinct checkpoints, E10.5, E16.5, and P1. These distinct time points have helped delineate the molecular pathways and regulation of necroptosis. The embryonic lethality at E10.5 seen in knockouts of caspase-8, FADD, or FLIP (cflar), components of the extrinsic apoptosis pathway, resulted in pallid embryos that did not exhibit the expected cellular expansions. This was the first suggestion that these factors play an important role in the inhibition of necroptotic cell death. The embryonic lethality at E16.5 highlighted the importance of TNF engaging necroptosis in vivo, since elimination of TNFR1 from casp8 (-/-), fadd (-/-), or cflar (-/-), ripk3 (-/-) embryos delayed embryonic lethality from E10.5 until E16.5. The P1 checkpoint demonstrates the dual role of RIPK1 in both the induction and inhibition of necroptosis, depending on the upstream signal. This review summarizes the role of necroptosis in development and the genetic evidence that helped detail the molecular mechanisms of this novel pathway of programmed cell death.

Indexed as

AnimalsApoptosisCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell DifferentiationEmbryonic DevelopmentFas-Associated Death Domain ProteinHumansMiceNecrosisReceptor-Interacting Protein Serine-Threonine KinasesCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cflar protein, mouseFas-Associated Death Domain ProteinReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouseRipk3 protein, mouseCaspase-8DevelopmentNecroptosisRIPK3

Identifiers

PMID27056574
PMCPMC11108279

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.