Kai Er Eng

TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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: A novel mechanism for SG disruption is described usingSemliki Forest virus nsP3 sequesters G3BP to inhibit stress granule formation on viral mRNAs and the efficient translation of viral mRNA containing a translation enhancer element assists disruption of SGs in infected cells.

TL;DR: A straightforward assay for autophagy is presented which combines the sensitivity of the EGFP-LC3 reporter protein with the throughput capacity and quantitative power of flow cytometry and is extended to the detection of autophagosome formation in non-transfected cells.

TL;DR: It is found thatSFV infection, unlike nutrient starvation, did not inactivate the constitutive negative regulator of autophagosome formation, mammalian target of rapamycin, suggesting that SFV-dependent accumulation of Autophagosomes was not a result of enhanced autophagy formation.

TL;DR: It is concluded that blockage of autophagic flux by tenovins is necessary to eliminate melanoma cells that survive B-Raf inhibition and achieve total tumour cell kill and that autophagy blockage can be achieved at a lower concentration than by chloroquine.