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.
The cAMP-dependent protein kinase A controls the switch from actively sprouting new blood vessel formation to vessel quiescence by reducing endothelial autophagy through phosphorylation-mediated destabilisation of ATG16L1.
The dynamic phosphorylation of autophagy component WIPI2B is critical to maintain autophagosome biogenesis in neurons, and ectopic expression of WIPI2B can restore rates of autophagosome biogenesis in aged neurons.
Proteasomes are protected from autophagic elimination upon carbon starvation by sequestration into cytoplasmic storage granules, which aid cell fitness by providing a cache of proteasomes that can be rapidly remobilized when carbon availability improves.
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.