Starving Intestinal Inflammation with the Amino Acid Sensor GCN2

Xavier S Revelo; Shawn Winer; Daniel A Winer

doi:10.1016/j.cmet.2016.04.020

Starving Intestinal Inflammation with the Amino Acid Sensor GCN2

Cell Metab. 2016 May 10;23(5):763-5. doi: 10.1016/j.cmet.2016.04.020.

Authors

Xavier S Revelo¹, Shawn Winer², Daniel A Winer³

Affiliations

¹ Diabetes Research Group, Division of Cellular & Molecular Biology, Toronto General Research Institute (TGRI), University Health Network, Toronto, ON M5G 1L7, Canada.
² Diabetes Research Group, Division of Cellular & Molecular Biology, Toronto General Research Institute (TGRI), University Health Network, Toronto, ON M5G 1L7, Canada; Department of Laboratory Medicine, St. Michael's Hospital, Toronto, ON M5B 1W8, Canada.
³ Diabetes Research Group, Division of Cellular & Molecular Biology, Toronto General Research Institute (TGRI), University Health Network, Toronto, ON M5G 1L7, Canada; Department of Pathology, University Health Network, Toronto, ON M5G 2C4, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada; Department of Immunology, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address: dan.winer@uhn.ca.

PMID: 27166939
DOI: 10.1016/j.cmet.2016.04.020

Abstract

Metabolic stressors are emerging as important controls over immune system function. In a recent paper, Ravindran et al. (2016) uncovered a novel mechanism by which an amino acid sensing pathway controls inflammation in the gut.

MeSH terms

Amino Acids / metabolism*
Animals
Autophagy
Inflammation / metabolism
Inflammation / pathology*
Intestinal Mucosa / metabolism
Intestines / pathology*
Mice
Models, Biological
Protein Serine-Threonine Kinases / metabolism*

Substances

Amino Acids
Eif2ak4 protein, mouse
Protein Serine-Threonine Kinases