Vojo Deretic

TL;DR: In this paper, the integral membrane protein ATG9A plays a key role in autophagy and is present in numerous compartments, including the plasma membrane (PM), but the reasons for its distribution to the PM and its role at the PM are not understood.

TL;DR: A protocol to quantify autophagic degradation of longlived proteins in macrophages is described, based on a pulse-chase approach, whereby cellular proteins are radiolabeled by an isotopically marked amino acid, the short-lived, rapidly turned over, proteins are allowed to be degraded during a long chase period, and then the remaining, stable radolabeled proteins are subjected to autophotic degradation.

TL;DR: The endosomal hyperacidification and excessive proinflammatory response in CF are in part due to deficiencies in NO‐ and cGMP‐regulated processes and can be pharmacologically reversed using PDE5 inhibitors.

TL;DR: It is shown that inhibiting MTORC1 by RPTOR deficiency led to autophagic sequestration of lipid droplets, formation of LD-containing lysosomes, and elevation of basal and isoproterenol-induced lipolysis in vivo and in primary adipocytes.

TL;DR: This review addresses the advantages and disadvantages of delivering drugs to induce autophagy in M. tuberculosis-infected macrophages and term here this (still experimental) approach, of compartment-targeting, autophagic-based, host-directed therapy as "Track-II antituberculosis chemotherapy."