dc.creatorLovy, Alenka
dc.creatorFoskett, J. Kevin
dc.creatorCárdenas, César
dc.date.accessioned2018-03-06T15:25:19Z
dc.date.available2018-03-06T15:25:19Z
dc.date.created2018-03-06T15:25:19Z
dc.date.issued2016-06
dc.identifierMolecular & Cellular Oncology 2016, VOL. 3, NO. 4, e1185563 (2 pages)
dc.identifier2372-3556
dc.identifier10.1080/23723556.2016.1185563
dc.identifierhttps://repositorio.uchile.cl/handle/2250/146715
dc.description.abstractMitochondrial metabolism is essential to fulfill the large demand for macromolecule biosynthesis in cancer. We recently identified low-level InsP3R-mediated Ca2+ transfer to mitochondria as an unexpected requirement for mitochondrial function. Here we reveal that its absence specifically targets cancer cells and causes necrosis at daughter cell separation during ongoing proliferation.
dc.languageen
dc.publisherTaylor & Francis
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceMolecular & Cellular Oncology
dc.subjectOXPHOS
dc.subjectnecrosis
dc.subjectMCU
dc.subjectcell cycle
dc.subjectautophagy
dc.subjectAMPK
dc.titleInsP3R, the calcium whisperer: Maintaining mitochondrial function in cancer
dc.typeArtículo de revista


Este ítem pertenece a la siguiente institución