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Authordc.contributor.authorLovy, Alenka 
Authordc.contributor.authorFoskett, J. Kevin 
Authordc.contributor.authorCárdenas, César 
Admission datedc.date.accessioned2018-03-06T15:25:19Z
Available datedc.date.available2018-03-06T15:25:19Z
Publication datedc.date.issued2016-06
Cita de ítemdc.identifier.citationMolecular & Cellular Oncology 2016, VOL. 3, NO. 4, e1185563 (2 pages)es_ES
Identifierdc.identifier.issn2372-3556
Identifierdc.identifier.other10.1080/23723556.2016.1185563
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/146715
Abstractdc.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.es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherTaylor & Francises_ES
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 & Cellular Oncologyes_ES
Keywordsdc.subjectOXPHOSes_ES
Keywordsdc.subjectnecrosises_ES
Keywordsdc.subjectMCUes_ES
Keywordsdc.subjectcell cyclees_ES
Keywordsdc.subjectautophagyes_ES
Keywordsdc.subjectAMPKes_ES
Títulodc.titleInsP3R, the calcium whisperer: Maintaining mitochondrial function in canceres_ES
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorcrbes_ES


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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