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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
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Amino acids and mTOR signalling in anabolic function.

C G Proud1

  • 1Department of Biochemistry and Molecular Biology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada V6T 1Z3. cgpr@interchange.ubc.ca

Biochemical Society Transactions
|October 25, 2007
PubMed
Summary

Amino acids, especially leucine, control protein synthesis and cell growth by regulating the mTORC1 pathway. Understanding how cells sense amino acids to activate mTORC1 is crucial for cell biology research.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Amino acids are critical nutrients that regulate cellular processes.
  • The mammalian target of rapamycin, complex 1 (mTORC1) pathway is a central regulator of cell growth, proliferation, and metabolism.
  • mTORC1 integrates signals from nutrients, growth factors, and energy status to control protein synthesis and ribosome biogenesis.

Purpose of the Study:

  • To review the mechanisms by which intracellular amino acids regulate mTORC1 signaling.
  • To highlight the role of specific amino acids, such as leucine, in mTORC1 activation.
  • To discuss the dissociation of amino acid-dependent mTORC1 regulation from the TSC1/2 complex pathway.

Main Methods:

  • Review of existing literature on amino acid sensing and mTORC1 signaling.
  • Analysis of studies investigating the molecular players involved in amino acid-mediated mTORC1 activation.
  • Comparison of amino acid-dependent mTORC1 regulation with growth factor-dependent pathways.

Main Results:

  • Amino acids, particularly leucine, potently activate mTORC1.
  • Amino acid-induced mTORC1 activation occurs independently of the tuberous sclerosis complex 1/2 (TSC1/2) complex.
  • Specific intracellular amino acid pools and sensing mechanisms are key to mTORC1 regulation.

Conclusions:

  • Intracellular amino acid availability is a critical signal for mTORC1 activation, controlling protein synthesis and ribosome biogenesis.
  • The mechanisms of amino acid sensing and subsequent mTORC1 regulation are distinct from those activated by growth factors like insulin.
  • Further research into these pathways will elucidate fundamental aspects of cellular anabolism and metabolic control.