Evidence map›Paper›PMID 27551516›Full record

ArticleCell death discovery2016

Caspase-mediated cleavage of raptor participates in the inactivation of mTORC1 during cell death.

R Martin, C Desponds, R O Eren, M Quadroni, M Thome, N Fasel

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  4. Review
  5. Cardamonin inhibits cell proliferation by caspase-mediated cleavage of Raptor.Naunyn-Schmiedeberg's archives of pharmacology · 2021
    Article
  6. Crosstalk of the Caspase Family and Mammalian Target of Rapamycin Signaling.International journal of molecular sciences · 2021
    Review
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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

6 authors at 1 institution in 1 country.

R MartinDepartment of Biochemistry, University of Lausanne , Vaud, Switzerland.
C DespondsDepartment of Biochemistry, University of Lausanne , Vaud, Switzerland.
R O ErenDepartment of Biochemistry, University of Lausanne , Vaud, Switzerland.
M QuadroniDepartment of Biochemistry, University of Lausanne, Vaud, Switzerland; Protein Analysis Facility (PAF), Centre Intégratif de Génomique, Quartier UNIL-Sorge, University of Lausanne, Lausanne , Switzerland.
M ThomeDepartment of Biochemistry, University of Lausanne , Vaud, Switzerland.ORCID 0000-0002-5656-2139
N FaselDepartment of Biochemistry, University of Lausanne , Vaud, Switzerland.
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian target of rapamycin complex 1 (mTORC1) is a highly conserved protein complex regulating key pathways in cell growth. Hyperactivation of mTORC1 is implicated in numerous cancers, thus making it a potential broad-spectrum chemotherapeutic target. Here, we characterized how mTORC1 responds to cell death induced by various anticancer drugs such rapamycin, etoposide, cisplatin, curcumin, staurosporine and Fas ligand. All treatments induced cleavage in the mTORC1 component, raptor, resulting in decreased raptor-mTOR interaction and subsequent inhibition of the mTORC1-mediated phosphorylation of downstream substrates (S6K and 4E-BP1). The cleavage was primarily mediated by caspase-6 and occurred at two sites. Mutagenesis at one of these sites, conferred resistance to cell death, indicating that raptor cleavage is important in chemotherapeutic apoptosis.

Identifiers

PMID27551516
PMCPMC4979510
OpenAlexW2340438210

What OpenQuestion holds

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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.