Autophagy in Disease and Therapy

This study shows that DIM induces apoptosis and autophagy in fission yeast in a dose-dependent manner, with autophagy contributing to cell survival against DIM.

This study shows that TBCK mutations impair mitochondrial quality control via lysosomal dysfunction, correlating with neurodegeneration severity.

This study shows that KANSL1 deficiency leads to oxidative stress-induced autophagy, causing synaptic dysfunction and neuronal network impairments in neurons.

This study shows that LC3B phosphorylation by STK4 regulates FYCO1 binding and directional transport of autophagosomes, switching their movement from retrograde to anterograde under starvation conditions.

This study identifies Gpnmb as a modifier of lysosome function in macrophages using QTL analysis in an AKR/JxDBA/2J intercross, showing its impact on proteolysis but not cholesterol metabolism.

This study shows that V-ATPase inhibition reduces tumor growth and restores autophagy in a Drosophila glioma model and human glioblastoma neurospheres.

This study shows that autophagy genes atg7 and beclin1 are critical for energy metabolism and survival during the larval-to-juvenile transition in zebrafish, as their loss leads to early death due to metabolic stress.

This study shows that stigmasterol protects hippocampal neurons from hypoxia-reoxygenation injury by inducing mitophagy through LXRβ activation.

This study shows that neuronal autophagy regulates axonal ER calcium stores to control neurotransmission and postnatal viability in mice.

The paper shows that ATP/ADP levels and autophagy interact to regulate neuronal migration by controlling cell pausing and focal adhesion recycling in mice.

The paper assesses ULK1 kinase alterations across 30+ cancer types using -omics data and structural analysis, finding downregulation in gynecological tumors and significant mutation impacts on protein stability.

The paper identifies distinct regulatory mechanisms and functions of ULK1 and ULK2, showing they are less redundant than previously thought.

The paper identifies bulk autophagy and β-oxidation as critical energy providers during acute glucose starvation in yeast.

This study shows that Trichoplein regulates endothelial cell function by controlling autophagy, with implications for vascular health and coronary artery disease.

The paper shows that during human retinal ganglion cell differentiation, the mitochondrial degradation pathway shifts from the ubiquitine-proteasome system to the endo-lysosomal pathway, which is critical for cell survival.

The paper performs a quantitative systems pharmacology analysis of 225 autophagy modulators to uncover their molecular mechanisms and regulatory pathways.

This study shows SESN2 localizes to mitochondria and directly regulates mitochondrial functions independently of mTORC1.

This study determines the structural basis of p62/SQSTM1 PB1 domain filaments, their role in phase-separated p62 bodies, and their importance in cargo recognition and lysosomal targeting.

This study shows SIPA1L2 connects TrkB-containing amphisomes to dynein for retrograde trafficking and local signaling at presynaptic terminals, essential for BDNF-dependent plasticity.

This study identifies Rhes as a striatal-enriched protein that promotes mitophagy via Nix, contributing to striatal vulnerability in the brain.

This study shows that WIPI2B expression counteracts age-related decline in autophagosome biogenesis in neurons, suggesting it as a therapeutic target for age-associated neurodegeneration.

This study shows that AP-4 deficiency in mice causes axonal and autophagosome biogenesis defects by impairing ATG9A sorting from the trans-Golgi network.

This study shows ULK1 phosphorylates ATG16L1, enhancing wildtype function but destabilizing the Crohn’s disease-associated mutant, thereby affecting xenophagy.

This study identifies vault RNA1-1 as a riboregulator of autophagy by interacting with p62, showing that it modulates autophagic flux.

This paper investigates the molecular properties of Arabidopsis autophagy cargo receptors ATI1 and ATI2, showing their intrinsically disordered regions and post-translational modifications upon ATG8 interaction.

The paper integrates proteomic and transcriptomic data from intestinal organoids to identify autophagy-dependent processes in Paneth cells, showing that autophagy impairment affects protein abundance and key cellular functions.

This paper builds a computational model to study how cells decide between autophagy and apoptosis under stress, revealing that cytoplasmic Ca2+ acts as a rheostat regulated by G-protein signaling and AMPK.