Michal H. Mudd

TL;DR: The cooperation between TRIM16 and Galectin-3 in targeting and activation of selective autophagy protects cells from lysosomal damage and Mycobacterium tuberculosis invasion.

TL;DR: It is shown that in response to lysosomal damage, the prototypical cytosolic secretory autophagy cargo IL‐1β is recognized by specialized secretoryautosolic cargo receptor TRIM16 and that this receptor interacts with the R‐SNARE Sec22b to recruit cargo to the LC3‐II+ sequestration membranes.

TL;DR: Gal3, a β-galactoside-binding cytosolic lectin, unifies and coordinates ESCRT and autophagy responses to lysosomal damage, which includes membrane repair, removal, and replacement.

TL;DR: It is shown that mTOR is inhibited by lysosomal damage, and a novel galectin-based signal-transduction system, termed here GALTOR, intersects with the known regulators of mTOR on theLysosome and controls them in response to lysOSomal damage.

TL;DR: Flubendazole is identified as a potent inducer of autophagy initiation and flux by affecting acetylated and dynamic microtubules in a reciprocal way, uncovering a new approach to inducing autophagic flux that may be applicable in disease treatment.