Evidence map›Paper›PMID 28411448›Full record

ReviewCurrent opinion in cell biology2017

mTORC1 signaling and the metabolic control of cell growth.

Issam Ben-Sahra, Brendan D Manning

Abstract readReview
In one paragraph

Review in Current opinion in cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 380 papers.

0numbers the graph read from it
0cells of the map it votes in
380citing 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

380 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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  6. Review
  7. Review
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  10. Article
  11. A TerminaTOR of mTORC1 signaling.Nature chemical biology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

320 more citing papers are in PubMed but not listed here.

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

2 authors.

Issam Ben-SahraDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: issam.ben-sahra@northwestern.edu.
Brendan D ManningDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: bmanning@hsph.harvard.edu.

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Decoding and Targeting the PI3K-mTOR Signaling Network in CancerR35CA197459 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI BRENDAN D. MANNING · 2015 to 2026
$10.8M
Linking Oncogenic Signaling to Tumor MetabolismR00CA194192 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BEN-SAHRA, ISSAM · 2017 to 2019
$729k
Linking oncogenic signaling to tumor metabolismK99CA194192 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI BEN-SAHRA, ISSAM · 2015 to 2016
$195k
NCI NIH HHS K99 CA194192NCI NIH HHS P01 CA120964NCI NIH HHS R00 CA194192NCI NIH HHS R35 CA197459
6 · The paper itself

Abstract

mTOR [mechanistic target of rapamycin] is a serine/threonine protein kinase that, as part of mTORC1 (mTOR complex 1), acts as an important molecular connection between nutrient signals and the metabolic processes indispensable for cell growth. While there has been pronounced interest in the upstream mechanisms regulating mTORC1, the full range of downstream molecular targets through which mTORC1 signaling stimulates cell growth is only recently emerging. It is now evident that mTORC1 promotes cell growth primarily through the activation of key anabolic processes. Through a diverse set of downstream targets, mTORC1 promotes the biosynthesis of macromolecules, including proteins, lipids, and nucleotides to build the biomass underlying cell, tissue, and organismal growth. Here, we focus on the metabolic functions of mTORC1 as they relate to the control of cell growth. As dysregulated mTORC1 underlies a variety of human diseases, including cancer, diabetes, autoimmune diseases, and neurological disorders, understanding the metabolic program downstream of mTORC1 provides insights into its role in these pathological states.

Indexed as

Signal TransductionAnimalsCell CycleCell ProliferationHumansMechanistic Target of Rapamycin Complex 1Metabolic Networks and PathwaysMultiprotein ComplexesProtein Serine-Threonine KinasesTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProtein Serine-Threonine KinasesTOR Serine-Threonine Kinases

Identifiers

PMID28411448
PMCPMC5545101

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.