Evidence map›Paper›PMID 33635313›Full record

ArticleThe Journal of cell biology2021

mTORC1 activity is supported by spatial association with focal adhesions.

Yoana Rabanal-Ruiz, Adam Byron, Alexander Wirth, Ralitsa Madsen, Lucia Sedlackova, Graeme Hewitt, Glyn Nelson, Julian Stingele, Jimi C Wills, Tong Zhang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  8. Perturbation of METTL1-mediated tRNA NNature communications · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 9 institutions in 3 countries.

Yoana Rabanal-Ruiz *Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Adam Byron *Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
Alexander WirthCellular Neurophysiology, Hannover Medical School, Hannover, Germany.
Ralitsa MadsenUCL Cancer Institute, University College London, London, UK.
Lucia SedlackovaBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Graeme HewittDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Glyn NelsonBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Julian StingeleGene Center, Ludwig Maximilians University Munich, Munich, Germany.
Jimi C WillsCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
Tong ZhangWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
André ZeugCellular Neurophysiology, Hannover Medical School, Hannover, Germany.
Reinhard FässlerDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Bart VanhaesebroeckUCL Cancer Institute, University College London, London, UK.
Oliver D K MaddocksWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
Evgeni PonimaskinCellular Neurophysiology, Hannover Medical School, Hannover, Germany.
Bernadette CarrollSchool of Biochemistry, University of Bristol, Bristol, UK.
Viktor I KorolchukBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Newcastle University · GBMedizinische Hochschule Hannover · DEEdinburgh Cancer Research · GBUniversity College London · GBUniversity of Glasgow · GBLudwig-Maximilians-Universität München · DEMax Planck Institute of Biochemistry · DEThe Francis Crick Institute · GBUniversity of Bristol · GB

Funding

Biotechnology and Biological Sciences Research CouncilCancer Research UK 15965Cancer Research UK 25722Cancer Research UK C53309/A19702European Research Council 801750Wellcome TrustWellcome Trust 218547/Z/19/Z
6 · The paper itself

Abstract

The mammalian target of rapamycin complex 1 (mTORC1) integrates mitogenic and stress signals to control growth and metabolism. Activation of mTORC1 by amino acids and growth factors involves recruitment of the complex to the lysosomal membrane and is further supported by lysosome distribution to the cell periphery. Here, we show that translocation of lysosomes toward the cell periphery brings mTORC1 into proximity with focal adhesions (FAs). We demonstrate that FAs constitute discrete plasma membrane hubs mediating growth factor signaling and amino acid input into the cell. FAs, as well as the translocation of lysosome-bound mTORC1 to their vicinity, contribute to both peripheral and intracellular mTORC1 activity. Conversely, lysosomal distribution to the cell periphery is dispensable for the activation of mTORC1 constitutively targeted to FAs. This study advances our understanding of spatial mTORC1 regulation by demonstrating that the localization of mTORC1 to FAs is both necessary and sufficient for its activation by growth-promoting stimuli.

Indexed as

Amino AcidsAnimalsCell LineCell Line, TumorCell MembraneFocal AdhesionsHeLa CellsHumansIntracellular MembranesLysosomesMechanistic Target of Rapamycin Complex 1MiceSignal TransductionAmino AcidsMechanistic Target of Rapamycin Complex 1

Identifiers

PMID33635313
PMCPMC7923692
OpenAlexW3130488722

What OpenQuestion holds

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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.