The pseudoenzyme CPT1C is able to sense changes in intracellular malonyl-CoA levels caused by nutrients or energy stress and regulate late endosomes/lysosomes anterograde transport, necessary for proper axon growth.
Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.
Genetic analysis of a CLN4 Drosophila model suggests that the disease-causing alleles act as dominant gain of function mutations that cause CSPα oligomerization and impair secretory and prelysosomal trafficking.
The polarity protein crumbs controls apical secretion and the architecture of the apical domain by modulating PI(4,5)P2 levels and the organization of apical Rab6-, Rab11-, and Rab30-dependent trafficking.
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.
Structure-based virtual screening reveals multiple novel TRPV5 inhibitors that bind and exert their effect from previously unidentified binding sites as characterized by cryo-electron microscopy and electrophysiology.