Evidence map›Paper›PMID 29119228›Full record

ReviewCellular and molecular life sciences : CMLS2018

Macropinocytosis, mTORC1 and cellular growth control.

Sei Yoshida, Regina Pacitto, Ken Inoki, Joel Swanson

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Plasminogen Activator Inhibitor-1 is Internalized by Endothelial Cells via A Pinocytosis-Like Mechanism and Evades Degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Macropinosomes are a site of HIV-1 entry into primary CD4Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. EGF-Induced Macropinocytosis Promotes NAV1-Dependent Internalization of Occludin in Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Insights of Endocytosis Signaling in Health and Disease.International journal of molecular sciences · 2023
    Review
  17. Chaperone-assisted selective autophagy targets filovirus VP40 as a client and restricts egress of virus particles.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Review
  19. Actin dynamics in protein homeostasis.Bioscience reports · 2022
    Review
  20. Article
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

4 authors at 1 institution in 1 country.

Sei YoshidaDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, 48109-5620, USA.
Regina PacittoDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, 48109-5620, USA.
Ken InokiDepartment of Integrative and Molecular Physiology and Internal Medicine, Life Sciences Institute, University of Michigan, Ann Arbor, MI, 48109, USA.
Joel SwansonDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, 48109-5620, USA. jswan@umich.edu.ORCID http://orcid.org/0000-0003-0900-8212
University of Michigan · US

Funding

Role of TSC-mTORC1 pathway for podocyte injury in diabetic nephropathyR01DK083491 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI INOKI, KEN · 2009 to 2017
$3.0M
Lysosomal cholesterol-dependent anabolic regulationR01DK124709 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI INOKI, KEN · 2022 to 2025
$2.1M
The Regulation of MacropinocytosisR01GM110215 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SWANSON, JOEL A · 2014 to 2017
$1.3M
Molecular mechanism of mTORC1-dependent translation and ribosome biogenesisR01GM110019 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI INOKI, KEN · 2015 to 2018
$1.2M
NIDDK NIH HHS DK083491NIDDK NIH HHS R01 DK083491NIDDK NIH HHS R01 DK124709NIGMS NIH HHS GM110019NIGMS NIH HHS GM110215NIGMS NIH HHS R01 GM110019NIGMS NIH HHS R01 GM110215U.S. Department of Defense TS140055
6 · The paper itself

Abstract

The growth and proliferation of metazoan cells are driven by cellular nutrient status and by extracellular growth factors. Growth factor receptors on cell surfaces initiate biochemical signals that increase anabolic metabolism and macropinocytosis, an actin-dependent endocytic process in which relatively large volumes of extracellular solutes and nutrients are internalized and delivered efficiently into lysosomes. Macropinocytosis is prominent in many kinds of cancer cells, and supports the growth of cells transformed by oncogenic K-Ras. Growth factor receptor signaling and the overall metabolic status of the cell are coordinated in the cytoplasm by the mechanistic target-of-rapamycin complex-1 (mTORC1), which positively regulates protein synthesis and negatively regulates molecular salvage pathways such as autophagy. mTORC1 is activated by two distinct Ras-related small GTPases, Rag and Rheb, which associate with lysosomal membranes inside the cell. Rag recruits mTORC1 to the lysosomal surface where Rheb directly binds to and activates mTORC1. Rag is activated by both lysosomal luminal and cytosolic amino acids; Rheb activation requires phosphoinositide 3-kinase, Akt, and the tuberous sclerosis complex-1/2. Signals for activation of Rag and Rheb converge at the lysosomal membrane, and several lines of evidence support the idea that growth factor-dependent endocytosis facilitates amino acid transfer into the lysosome leading to the activation of Rag. This review summarizes evidence that growth factor-stimulated macropinocytosis is essential for amino acid-dependent activation of mTORC1, and that increased solute accumulation by macropinocytosis in transformed cells supports unchecked cell growth.

Indexed as

Amino AcidsAnimalsCell ProliferationHumansIntercellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1PinocytosisSignal TransductionAmino AcidsIntercellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1CancerMacropinocytosismTORC1PhosphoinositideSmall GTPase

Identifiers

PMID29119228
PMCPMC5843684
OpenAlexW2768016017

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.