Fine tuning PERK signaling to control cell fate under stress
Author
dc.contributor.author
Urra, Hery
Author
dc.contributor.author
Hetz Flores, Claudio
Admission date
dc.date.accessioned
2018-06-29T14:58:32Z
Available date
dc.date.available
2018-06-29T14:58:32Z
Publication date
dc.date.issued
2017
Cita de ítem
dc.identifier.citation
Nature Structural & Molecular Biology, volume 24 number 10 October 2017
es_ES
Identifier
dc.identifier.other
10.1038/nsmb.3478
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/149348
Abstract
dc.description.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.
es_ES
Patrocinador
dc.description.sponsorship
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