Cited by 778PI3K/AKT/mTOR signaling in cancerMuscle metabolism and nutritionRNA and protein synthesis mechanisms

The mTOR pathway in the control of protein synthesis

Wang, Xuemin, Proud, Christopher G.·2006·Physiology

Abstract

Signaling through mammalian target of rapamycin (mTOR) is activated by amino acids, insulin, and growth factors, and impaired by nutrient or energy deficiency. mTOR plays key roles in cell physiology. mTOR regulates numerous components involved in protein synthesis, including initiation and elongation factors, and the biogenesis of ribosomes themselves.

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Crossref · 10.1152/physiol.00024.2006

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57 of 57 references verified0 citation errors · 0 not checkable

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Authors
Wang, X., & Proud, C. G.
Affiliations
University of British Columbia (CA)
Venue
Physiology
Published
2006-10
Volume
21
Issue
5
Pages
362-369
ISSN
  • 0886-1714 (ISSN-L)
  • 1548-9213
  • 1548-9221
OpenAlex
W2158389310
Cited by
778
References
57
Citations by year
2026: 20 · 2025: 39 · 2024: 41 · 2023: 47 · 2022: 58 · 2021: 63 · 2020: 51 · 2019: 32 · 2018: 50 · 2017: 34 · 2016: 33 · 2015: 42 · 2014: 43 · 2013: 38 · 2012: 40
FWCI
2.11
Type
journal article
Language
en
Open access
closed
Locations
  • Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • ePrints Soton (University of Southampton) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
Keywords
mTOR signaling, protein synthesis, amino acid signaling, insulin signaling, growth factor signaling, nutritional deficiency, energy deficiency, translation initiation factors, translation elongation factor, ribosome biogenesis
MeSH terms
Animals, Cell Physiological Phenomena, Humans, Protein Kinases, Ribosomes, Protein Biosynthesis, Signal Transduction, TOR Serine-Threonine Kinases

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