Evidence map›Paper›PMID 26159692›Full record

ReviewTrends in cell biology2015

Regulation of mTORC1 by PI3K signaling.

Christian C Dibble, Lewis C Cantley

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 489 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
489citing papers in PubMed, 3 pooled it
33.0field-weighted citation impact, top 1% 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

489 citing papers in PubMed, 3 syntheses or guidelines pooled it, 831 citations in OpenAlex.

  1. Pooled it
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  13. Enhancement of Therapeutic mRNA Translation in Cellular Stress Conditions.International journal of molecular sciences · 2026
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429 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 at 2 institutions in 1 country.

Christian C DibbleDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Lewis C CantleyMeyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. Electronic address: lcantley@med.cornell.edu.
Cornell University · USHarvard University · US

Funding

The Role of PI3K in Growth RegulationR01GM041890 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI CANTLEY, LEWIS C. · 1990 to 2016
$4.1M
ROLE OF VITAMIN B5 AND COENZYME A METABOLISM IN PI3K DRIVEN TUMORIGENESISK99CA194314 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DIBBLE, CHRISTIAN · 2015 to 2016
$339k
NCI NIH HHS K99 CA194314NCI NIH HHS K99-CA194314NIGMS NIH HHS R01 GM041890NIGMS NIH HHS R01-GM041890
6 · The paper itself

Abstract

The class I phosphoinositide 3-kinase (PI3K)-mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) signaling network directs cellular metabolism and growth. Activation of mTORC1 [composed of mTOR, regulatory-associated protein of mTOR (Raptor), mammalian lethal with SEC13 protein 8(mLST8), 40-kDa proline-rich Akt substrate (PRAS40), and DEP domain-containing mTOR-interacting protein (DEPTOR)] depends on the Ras-related GTPases (Rags) and Ras homolog enriched in brain (Rheb) GTPase and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin). Here we discuss the signal transduction mechanisms through which growth factor-responsive PI3K signaling activates mTORC1. We focus on how PI3K-dependent activation of Akt and spatial regulation of the tuberous sclerosis complex (TSC) complex (TSC complex) [composed of TSC1, TSC2, and Tre2-Bub2-Cdc16-1 domain family member 7 (TBC1D7)] switches on Rheb at the lysosome, where mTORC1 is activated. Integration of PI3K- and amino acid-dependent signals upstream of mTORC1 at the lysosome is detailed in a working model. A coherent understanding of the PI3K-mTORC1 network is imperative as its dysregulation has been implicated in diverse pathologies including cancer, diabetes, autism, and aging.

Indexed as

Signal TransductionAnimalsAutistic DisorderDiabetes MellitusFeedback, PhysiologicalHumansInsulinIntracellular Signaling Peptides and ProteinsLysosomesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesInsulinIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesinsulinlysosomeRagRaptorRhebTSC2

Identifiers

PMID26159692
PMCPMC4734635
OpenAlexW1804602290

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.