Abstract
PERK is a major sensor of the unfolded protein response controlling cell fate under endoplasmic reticulum (ER) stress. A new study reveals an additional step for optimal PERK signaling, involving the binding of CNPY2 to PERK's luminal domain. The PERK-CNPY2 axis was shown to enhance cell death under ER stress in vivo influence liver disease.
Patrocinador
FONDECYT
1140549
3160461
Millennium Institute
P09-015-F
FONDAP
15150012
U.S. Office of Naval Research-Global (ONR-G)
N62909-16-1-2003
U.S. Air Force Office of Scientific Research
FA9550-16-1-0384
BNI
Indexation
Artículo de publicación ISI