Evidence map›Paper›PMID 30598363›Full record

ArticleMolecular cell2019

RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation.

Gianmaria Liccardi, Laura Ramos Garcia, Tencho Tenev, Alessandro Annibaldi, Arnaud J Legrand, David Robertson, Rebecca Feltham, Holly Anderton, Maurice Darding, Nieves Peltzer and 15 more

Open access · hybridAbstract readVideo-Audio Media
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Targeting caspase-8/c-FLIPFrontiers in cell and developmental biology · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

25 authors at 11 institutions in 6 countries.

Gianmaria LiccardiThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
Laura Ramos GarciaThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
Tencho TenevThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
Alessandro AnnibaldiThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
Arnaud J LegrandThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
David RobertsonThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.
Rebecca FelthamThe Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, Victoria 3052, Australia.
Holly AndertonThe Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, Victoria 3052, Australia.
Maurice DardingThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK; Centre for Cell Death, Cancer, and Inflammation (CCCI), UCL Cancer Institute, University College, London WC1E 6BT, UK.
Nieves PeltzerCentre for Cell Death, Cancer, and Inflammation (CCCI), UCL Cancer Institute, University College, London WC1E 6BT, UK.
Marius DannappelInstitute for Genetics, Centre for Molecular Medicine (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Hannah SchünkeInstitute for Genetics, Centre for Molecular Medicine (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Luca L FavaDivision of Dev. Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, A-6020, Austria.
Manuel D HaschkaDivision of Dev. Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, A-6020, Austria.
Timo GlatterProteomics Core Facility, Biocentrum of the University of Basel, Basel, Switzerland; Max Planck Institute for Terrestrial Microbiology, Karl-von-Frisch Str. 10, 35043 Marburg, Germany.
Alexey NesvizhskiiDepartment of Pathology, Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI, USA.
Alexander SchmidtProteomics Core Facility, Biocentrum of the University of Basel, Basel, Switzerland.
Philip A HarrisPattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, PA 19426, USA.
John BertinPattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, PA 19426, USA.
Peter J GoughPattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, PA 19426, USA.
Andreas VillungerDivision of Dev. Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, A-6020, Austria; Tyrolean Cancer Research Institute, A-6020 Innsbruck, Austria.
John SilkeInstitute for Genetics, Centre for Molecular Medicine (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Manolis PasparakisInstitute for Genetics, Centre for Molecular Medicine (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Katiuscia BianchiThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK; Barts Cancer Institute, Queen Mary, John Vane Science Centre, University of London, Charterhouse Square, London EC1M 6BQ, UK.
Pascal MeierThe Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, Mary-Jean Mitchell Green Building, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK. Electronic address: pmeier@icr.ac.uk.
Breast Cancer Now · GBGlaxoSmithKline (United States) · USCologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEInnsbruck Medical University · ATUniversity College London · GBUniversity of Basel · CHUniversity of Cologne · DEWalter and Eliza Hall Institute of Medical Research · AUInstitute of Cancer Research · GBUniversität Innsbruck · ATUniversity of Michigan–Ann Arbor · US

Funding

COMPUTATIONAL TOOLS FOR MASS SPECTROMETRY-BASED INTERACTOME DATAR01GM094231 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Alexey I Nesvizhskii · 2010 to 2026
$5.4M
Austrian Science Fund FWF I 1298Austrian Science Fund FWF P 26856Cancer Research UK 24399Medical Research Council G1000089Medical Research Council MR/M019217/1NIGMS NIH HHS R01 GM094231
6 · The paper itself

Abstract

Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 activating ripoptosome complexes, positively and negatively regulating apoptosis, necroptosis, and inflammation. Here, we report an unanticipated cell-death- and inflammation-independent function of RIPK1 and Caspase-8, promoting faithful chromosome alignment in mitosis and thereby ensuring genome stability. We find that ripoptosome complexes progressively form as cells enter mitosis, peaking at metaphase and disassembling as cells exit mitosis. Genetic deletion and mitosis-specific inhibition of Ripk1 or Caspase-8 results in chromosome alignment defects independently of MLKL. We found that Polo-like kinase 1 (PLK1) is recruited into mitotic ripoptosomes, where PLK1's activity is controlled via RIPK1-dependent recruitment and Caspase-8-mediated cleavage. A fine balance of ripoptosome assembly is required as deregulated ripoptosome activity modulates PLK1-dependent phosphorylation of downstream effectors, such as BUBR1. Our data suggest that ripoptosome-mediated regulation of PLK1 contributes to faithful chromosome segregation during mitosis.

Indexed as

Chromosomal InstabilityMitosisAneuploidyAnimalsApoptosisCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell Cycle ProteinsChromosome SegregationColonic NeoplasmsFas-Associated Death Domain ProteinFibroblastsHT29 CellsHumansInflammationMiceBub1b protein, mouseBUB1 protein, humanCASP8 and FADD-Like Apoptosis Regulating ProteinCASP8 protein, humanCasp8 protein, mouseCaspase 8Cell Cycle ProteinsCFLAR protein, humanCflar protein, mouseFADD protein, humanFadd protein, mouseFas-Associated Death Domain ProteinPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRipk1 protein, mouseBUBR1cancercaspase-8cell cyclecell deathchromosomal instabilitymitosisPLK1RIPK1ripoptosome

Identifiers

PMID30598363
PMCPMC6375735
OpenAlexW2907885025

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.