Amino acid regulation of autophagy through the GPCR TAS1R1-TAS1R3

Eric M. Wauson, Elma Zaganjor, Melanie H. Cobb

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

Cells require the ability to rapidly detect decreases in concentrations of free amino acids so that homeostatic mechanisms, including autophagy, can be engaged to replenish amino acids. Amino acids are transported into cells where it is generally accepted that they are detected by an intracellular sensor. We now show that the cell surface G protein coupled receptor (GPCR) TAS1R1-TAS1R3 (T1R1-T1R3) can sense extracellular amino acids, activate MTORC1, and inhibit autophagy. This receptor is expressed in most tissues and fasted TAS1R3 -/- mice have increased autophagy in the heart, skeletal muscle and liver.

Original languageEnglish (US)
Pages (from-to)418-419
Number of pages2
JournalAutophagy
Volume9
Issue number3
DOIs
StatePublished - Mar 2013

Keywords

  • Amino Acids
  • Ampk
  • Autophagy
  • Gpcr
  • Lysosome
  • Mtor
  • T1R1
  • T1R3
  • Ulk

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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