Our new studies show this is due to faulty trafficking of late endosomes to lysosomes, with concomitant homotypic fusion with the impacted vesicular compartments [five]. The defect in lysosome-directed trafficking also influences autophagic flux, with resultant accumulation of autophagosomes [five]. Eventually, the integrity with the cell membrane is compromised as https://charliex210qcp5.blogvivi.com/profile