Autophagy in Disease and Therapy

The paper shows that the human MLL-AF4 fusion protein induces autophagy and cell death in Drosophila fat body cells, contrasting its effect in the hematopoietic system.

This study identifies that vertical inhibition of the autophagy pathway enhances sensitivity to mTORC1 inhibition in PDAC, improving therapeutic efficacy.

The paper identifies ARMC1 as a repressor of mitophagy that interacts with TMEM11, BNIP3, and NIX, and shows TMEM11 antagonizes PPTC7 to protect receptors during mitophagy activation.

This study shows that ROS inhibit mitophagy by activating PARP1, which PARylates PINK1 and impairs its function.

This study shows rapamycin enhances autophagy and M2 microglial polarization by inhibiting the mTOR/ULK1 pathway in vivo and in vitro.

This study determines the crystal structure of Atg23 and identifies hydrophobic interactions between Atg23 and both N- and C-terminal regions of Atg9.

The paper shows that autophagy is suppressed in peripheral blood mononuclear cells of COPD patients, as indicated by reduced autophagic flux and fewer autophagy-related vacuoles.

This study shows that 2M* activates mitophagy and promotes EV release via LRP1 in erythroid cells, linking autophagy and vesicular trafficking.

This study shows that glucose levels in neuronal culture media affect PINK1-dependent mitophagy in human iNeurons, with BrainPhys medium reducing mitophagy compared to N2B27.

This paper identifies HRS as a regulator of lipid droplet catabolism in hepatocytes, showing it affects LD-lysosomal targeting and lysosomal function.

This paper identifies ORP3 as a lipid transfer protein that mediates lysosomal repair through interactions with LC3B and the TAK1-p38 signaling pathway.

This study shows that canonical autophagy remains inactive in iPSCs and NPCs under DNA damage, despite a functional autophagy machinery and responsive DNA damage response.

The paper reports a novel neurodevelopmental disorder caused by a frameshift mutation in ATG9B, and characterizes its effects using cell models and knock-in mice.

This study identifies ATG16L2 as a specialized regulator of VAIL-selective ATG8 lipidation, forming a functional heterodimer with ATG16L1.

This study identifies ATG7(2) as a driver of pancreatic cancer progression independent of autophagy, showing its role in promoting proliferation, migration, and tumor growth.

This study identifies sephin1's mechanism of action in proteostasis disruption by showing it binds G-actin, causes cytoskeleton misfolding, and modulates autophagy through mTORC1-TFEB and GCN2-eIF2-CHOP pathways.

This study shows Synphilin-1 helps cells survive proteotoxic stress by managing ubiquitinated protein aggregation and autophagy dysfunction in WHAMM/JMY knockout fibroblasts.

This study shows that declining autophagy in aged neurons leads to microtubule alterations, causing axonal and synaptic decay, and that enhancing autophagy can reverse these effects.

This paper determines the crystal structures of DFCP1's ATPase domain with ADP and ATP analogues, revealing structural elements that regulate ATP hydrolysis and omegasome dynamics.

This study identifies a multi-subunit autophagic capture complex that degrades ER-stalled MHC-I in pancreatic cancer, reducing immunogenicity.

This study uses two-photon imaging to show that mitophagy decreases with age in mouse somatosensory cortex neurons and astrocytes, with astrocytes showing higher mitophagy levels than neurons, and NAD+ treatment improves mitophagy in aged mice.

This study identifies EPG5 mutations causing neurodegeneration via mitochondrial dysfunction and innate immune activation in patient-derived cells.

This study shows that MITF regulates autophagy in RPE cells, with reduced MITF causing autophagy defects and lysosomal dysfunction linked to retinal degeneration.

The paper shows the V-ATPase/ATG16L1 axis is essential for de novo lumen formation during epithelial tube morphogenesis.

This study uses a Rosella-PLIN2 biosensor to track lipophagy in atherosclerosis, revealing cell-specific differences in lipid metabolism and immunometabolic interactions.

This study examines autophagy flux changes with age in human cell types, finding sex- and cell-type-specific patterns and a link to physical fitness.

This study quantifies basal autophagic flux in mice using GFP-LC3-RFP reporter mice, revealing higher flux in brain, liver, and kidney compared to other tissues.

This study identifies distinct mitophagy pathways in Muller glia and their role in retinal physiology and neurogenic transitions.

The paper develops a method to reposition lysosomes and identifies proteomic differences between perinuclear and peripheral lysosomes.