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Autophagy. 2013 Mar;9(3):418-9. doi: 10.4161/auto.22911. Epub 2012 Dec 7.

Amino acid regulation of autophagy through the GPCR TAS1R1-TAS1R3.

Author information

1
Department of Pharmacology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.

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.

KEYWORDS:

AMPK; GPCR; T1R1; T1R3; ULK; amino acids; autophagy; lysosome; mTOR

PMID:
23222068
PMCID:
PMC3590263
DOI:
10.4161/auto.22911
[Indexed for MEDLINE]
Free PMC Article

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