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Authordc.contributor.authorUrra, Hery 
Authordc.contributor.authorHetz Flores, Claudio 
Admission datedc.date.accessioned2019-01-29T14:47:55Z
Available datedc.date.available2019-01-29T14:47:55Z
Publication datedc.date.issued2014
Cita de ítemdc.identifier.citationMolecular Cell 54, May 22, 2014
Identifierdc.identifier.issn10974164
Identifierdc.identifier.issn10972765
Identifierdc.identifier.other10.1016/j.molcel.2014.05.013
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/160660
Abstractdc.description.abstractTumors 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.
Lenguagedc.language.isoen
Publisherdc.publisherCell Press
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceMolecular Cell
Keywordsdc.subjectMolecular Biology
Keywordsdc.subjectCell Biology
Títulodc.titleA Novel ER Stress-Independent Function of the UPR in Angiogenesis
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorlaj
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile