Sabrina Di Bartolomeo

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: It is shown that autophagy modulation regulates the migration and invasion capabilities of glioblastoma (GBM) cells, and that SNAIL and SLUG, two master regulators of the epithelial–mesenchymal transition (EMT process), were down‐regulated upon Autophagy stimulation and, as a consequence, a transcriptional and translational up‐regulation of N‐ and R‐cadherins was found.

TL;DR: It is shown that the scaffold protein AMBRA1 regulates cell proliferation by facilitating the dephosphorylation and degradation of the proto-oncogene c-Myc and that, when mTOR is inhibited, it enhances PP2A activity on this specific target, thereby reducing the cell division rate.