Marco Corazzari

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: It is shown that Ambra1 (activating molecule in Beclin1-regulated autophagy), a large, previously unknown protein bearing a WD40 domain at its amino terminus, regulatesAutophagy and has a crucial role in embryogenesis, and provides in vivo evidence supporting the existence of a complex interplay between autphagy, cell growth and cell death required for neural development in mammals.

TL;DR: When autophagy is induced, ULK1 phosphorylates AMBRA1, releasing the autophagic core complex from the cytoskeleton and allowing its relocalization to the ER membrane to nucleate autophagosome formation.

TL;DR: The results demonstrated that the autophagic flux is impaired in the liver from both NAFLD patients and murine models ofNAFLD, as well as in lipid-overloaded human hepatocytes, and it could be due to elevated ER stress leading to apoptosis.

TL;DR: It is found that p73 elicits apoptosis via the mitochondrial pathway using PUMA and Bax as mediators, and human ΔNp73, an isoform lacking the amino-terminal transactivation domain, inhibits TAp73-induced as well as p53-induced apoptosis.