The lysosome membrane is a new functional location for the ESCRTs in yeast.

Lysosomes are highly enriched in chloride, which is essential for their degradative function.

Transcription factors KLF2 and ETV1 repress the transcriptional program of mitochondrial biogenesis, resulting in impaired mitochondrial function in lysosomal storage diseases.

LAMP proteins, the major glycoproteins of the lysosome membrane, bind cholesterol directly and specifically, and interact with NPC1 and NPC2 proteins as part of the lysosomal cholesterol export process.

The lysosomal ion channel TPC2 emerges as an example of an ion channel in which ion selectivity is not fixed but rather agonist-selective.

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.

The endo-lysosomal system plays a positive essential role in the initiation of the cell cycle in yeast.

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.

Tricyclic antidepressants activate lysosomal two-pore Na⁺ channels in a voltage-dependent manner.