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Federica Di Sano

Researcher at University of Rome Tor Vergata

Publications -  21
Citations -  4186

Federica Di Sano is an academic researcher from University of Rome Tor Vergata. The author has contributed to research in topics: Endoplasmic reticulum & Reticulon. The author has an hindex of 14, co-authored 21 publications receiving 3223 citations. Previous affiliations of Federica Di Sano include Sapienza University of Rome.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

Endoplasmic Reticulum Stress Induces Apoptosis by an Apoptosome-dependent but Caspase 12-independent Mechanism *

TL;DR: It is shown here that in the absence of the apoptosome ER stress induces cytochrome c release from the mitochondria but that apoptosis cannot occur, and caspase 12, a protease until now believed to play a central role in the initiation of ER stress-induced cell death in the mouse system, is dispensable for the mitochondrial pathway of death to take place.
Journal ArticleDOI

Cell death and autophagy: cytokines, drugs, and nutritional factors.

TL;DR: The data exemplify that a given cell may flexibly respond to type and degree of (micro)environmental changes or cell death stimuli; a cell's response may shift gradually from the elimination of damaged proteins by autophagy and the recovery to autophagic or apoptotic pathways of cell death, the failure of which eventually may result in necrosis.