Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.
In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.
An ensemble of the ubiquitin-activating enzyme UBA6 and ubiquitin-conjugating enzyme/ubiquitin-ligase BIRC6 mediates ubiquitination of LC3, targeting the latter for proteasomal degradation and thus attenuating autophagic degradation of cellular substrates.
Erythroid-enriched BMP2K kinase, in addition to its predicted function in endocytosis, regulates distribution and abundance of COPII assemblies and autophagic degradation through opposing actions of its two splicing variants.
Impaired autophagy influences intestinal inflammation and hypersensitivity responses by orchestrating mucosal T cell populations, suggesting new translational perspectives for the treatment of these conditions.