| Literature DB >> 27203173 |
Lorenzo Galluzzi1, José Manuel Bravo-San Pedro2, Guido Kroemer3.
Abstract
In this issue of Molecular Cell, Park et al. (2016) elegantly demonstrate that a partial defect in autophagy supports malignant transformation as it favors the production of genotoxic reactive oxygen species by mitochondria.Entities:
Keywords: U2AF1(S34F); alternative splicing; autophagic flux; mutational rate; myelodysplastic syndrome; regulated cell death
Mesh:
Substances:
Year: 2016 PMID: 27203173 DOI: 10.1016/j.molcel.2016.05.001
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970