Lipophagy is the process of autophagic degradation of lipid droplets into fatty acids. Lipid droplets are coated with perilipin (PLIN) protiens and they need to be eliminated for the degradation of the lipids inside. Cytosolic Heat shock cognate 71 kDa protein (HSPA8) binds PLIN2 and PLIN3 on the lipid droplet surface. Consequently, PRKAA2 bind and phosphorylate perilipins targeting them for lipophagy (S Kaushik et al. 2015, S Kaushik et al. 2016). Experiments confirming this interaction were performed in mouse.
Lipophagy is the process of autophagic degradation of lipid droplets into fatty acids. Lipid droplets are coated with perilipin (PLIN) proteins and they need to be eliminated for the degradation of the lipids inside. Cytosolic Heat shock cognate 71 kDa protein (HSPA8) binds PLIN2 and PLIN3 on the lipid droplet surface. Subsequently, PRKAA2 binds and phosphorylates perilipins. Phosphorylated PLINs dissociate from PRKAA2 and are believed to translocate to the cytosol (S Kaushik et al. 2015, S Kaushik et al. 2016). Experiments suggesting this event were performed in mouse models.
Lipophagy is the process of autophagic degradation of lipid droplets into fatty acids. Lipid droplets are coated with perilipin (PLIN) proteins and they need to be eliminated for the degradation of the lipids inside. Cytosolic Heat shock cognate 71 kDa protein (HSPA8) binds PLIN2 and PLIN3 on the lipid droplet surface. Subsequently, AMPK binds and phosphorylates perilipins targeting them for lipophagy (S Kaushik et al. 2015, S Kaushik et al. 2016). The precise phosphorylation site(s) on PLINs are unknown. Experiments confirming this finding were performed in mouse models.
Once phosphorylated, PLINs are believed to dissociate from PRKAA2 and translocate to the cytosol (S Kaushik et al. 2015, S Kaushik et al. 2016). The precise dissociation mechanism of Plins is unclear. The experiments showing this finding were performed in mouse models.
Lipophagy is the process of autophagic degradation of lipid droplets into fatty acids. A key step in this process is the elimination of perilipin (PLIN) proteins on lipid droplet surface. This mechanism is initiated when the cytosolic Heat shock cognate 71 kDa protein (HSPA8) binds PLIN2 and PLIN3 on the lipid droplet surface. Consequently, perilipins are phosphorylated and targeted to degradation making the lipid available for hydrolysis (S Kaushik et al. 2015). Experiments confirming this interaction were performed in rats.