A Novel ER Stress-Independent Function of the UPR in Angiogenesis
Author
dc.contributor.author
Urra, Hery
Author
dc.contributor.author
Hetz Flores, Claudio
Admission date
dc.date.accessioned
2019-01-29T14:47:55Z
Available date
dc.date.available
2019-01-29T14:47:55Z
Publication date
dc.date.issued
2014
Cita de ítem
dc.identifier.citation
Molecular Cell 54, May 22, 2014
Identifier
dc.identifier.issn
10974164
Identifier
dc.identifier.issn
10972765
Identifier
dc.identifier.other
10.1016/j.molcel.2014.05.013
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/160660
Abstract
dc.description.abstract
Tumors rely on the unfolded protein response (UPR) and angiogenesis to survive the metabolic stress of hypoxia. Karali et al. (2014) revealed that VEGF signaling engages UPR sensors in an unconventional manner that is independent of endoplasmic reticulum (ER) stress, mediated by mTOR signaling to promote endothelial cell survival and angiogenesis.