Evidence map›Paper›PMID 32091387›Full record

ArticleeLife2020

Control of cell death/survival balance by the MET dependence receptor.

Leslie Duplaquet, Catherine Leroy, Audrey Vinchent, Sonia Paget, Jonathan Lefebvre, Fabien Vanden Abeele, Steve Lancel, Florence Giffard, Réjane Paumelle, Gabriel Bidaux and 4 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Leslie DuplaquetUniv. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.ORCID 0000-0002-6544-0432
Catherine Leroy *Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.
Audrey Vinchent *Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.
Sonia PagetUniv. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.
Jonathan LefebvreUniv. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.
Fabien Vanden AbeeleUniv. Lille, Inserm, U1003 - PHYCEL - Physiologie Cellulaire, Lille, France.ORCID 0000-0001-7111-7220
Steve LancelUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.ORCID 0000-0002-3292-5433
Florence GiffardNormandie Université, UNICAEN, INSERM U1086 ANTICIPE, UNICANCER, Cancer Centre F. Baclesse, Caen, France.
Réjane PaumelleUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.
Gabriel BidauxUniv. Lille, CNRS, UMR8523 - PhLAM - laboratoire de Physique des Lasers, Atomes et Molécules, Lille, France.ORCID 0000-0002-6162-3223
Laurent HeliotUniv. Lille, CNRS, UMR8523 - PhLAM - laboratoire de Physique des Lasers, Atomes et Molécules, Lille, France.
Laurent PoulainNormandie Université, UNICAEN, INSERM U1086 ANTICIPE, UNICANCER, Cancer Centre F. Baclesse, Caen, France.
Alessandro FurlanUniv. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.ORCID 0000-0001-6502-8416
David TulasneUniv. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies, Lille, France.ORCID 0000-0002-6764-7242
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

Institut National Du Cancer SIRIC OncoLilleRégion Hauts-de-France CPER Photonics
6 · The paper itself

Abstract

Control of cell death/survival balance is an important feature to maintain tissue homeostasis. Dependence receptors are able to induce either survival or cell death in presence or absence of their ligand, respectively. However, their precise mechanism of action and their physiological importance are still elusive for most of them including the MET receptor. We evidence that pro-apoptotic fragment generated by caspase cleavage of MET localizes to the mitochondria-associated membrane region. This fragment triggers a calcium transfer from endoplasmic reticulum to mitochondria, which is instrumental for the apoptotic action of the receptor. Knock-in mice bearing a mutation of MET caspase cleavage site highlighted that p40MET production is important for FAS-driven hepatocyte apoptosis, and demonstrate that MET acts as a dependence receptor in vivo. Our data shed light on new signaling mechanisms for dependence receptors' control of cell survival/death balance, which may offer new clues for the pathophysiology of epithelial structures.

Indexed as

AnimalsCell DeathCells, CulturedCell SurvivalEndoplasmic ReticulumHumansMiceMice, TransgenicMitochondriaProtein TransportProteolysisProto-Oncogene Proteins c-metProto-Oncogene Proteins c-metapoptosiscalciumcell biologyhepatocytemousereceptor tyrosine kinase

Identifiers

PMID32091387
PMCPMC7039684
OpenAlexW3008249097

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.