Our recent studies indicate that this is due to faulty trafficking of late endosomes to lysosomes, with concomitant homotypic fusion from the influenced vesicular compartments [five]. The defect in lysosome-directed trafficking also affects autophagic flux, with resultant accumulation of autophagosomes [5]. Eventually, the integrity of the cell membrane is compromised https://albertg207ydh0.blogdomago.com/profile