Coordinate control of lysosomal v-ATPase subunits and biogenesis factor TFEB by miR-1 identifies a key regulatory axis with strong links to age-related proteotoxic disease.

The ZNRF2 enzyme helps the mTOR protein complex to sense amino acid levels and regulate mammalian cell growth.

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.

ATP6V0A1 was identified as a key player in nephropathic cystinosis-related renal pathology, with antioxidants like ATX emerging as potential treatments to restore V0A1 expression, mitochondrial function, and balance autophagic processes.

The phagocytic receptor CED-1 is kept at the appropriate level by E3 ligase trim-21-mediated ubiquitination-proteasomal degradation for apoptotic cell clearance, which is independent of retromer-dependent recycling and lysosomal degradation.

The endoplasmic reticulum serves as a direct and primary source of calcium ions for the lysosome.

The AAA-ATPase VCP sustains sarcoplasmic proteostasis, in part, by controlling autophagosome-lysosome fusion and the integrity of a dynamic tubular lysosomal network.

Cell biological and genetic studies reveal age-associated alterations of lysosomes and modulation of lysosomal activity by longevity pathways.

Metformin extends C. elegans lifespan through lysosome-dependent coordination of TORC1 and AMPK pathways.