0000000001217005

AUTHOR

Thomas Juretschke

showing 3 related works from this author

RAB18 Loss Interferes With Lipid Droplet Catabolism and Provokes Autophagy Network Adaptations

2020

Autophagy is dependent on appropriate lipid supply for autophagosome formation. The regulation of lipid acquisition and the autophagy network response to lipid-limiting conditions are mostly elusive. Here, we show that the knockout of the RAB GTPase RAB18 interferes with lipid droplet catabolism, causing an impaired fatty acid release. The resulting reduced lipid-droplet-derived lipid availability influences autophagy and provokes adaptive modifications of the autophagy network. These adjustments include increased expression and phosphorylation of ATG2B as well as augmented formation of the ATG12-ATG5 conjugate. Moreover, ATG9A shows an enhanced phosphorylation at amino acid residues tyrosi…

rab3 GTP-Binding ProteinsImmunoblottingGTPaseReal-Time Polymerase Chain Reaction03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionStructural BiologyLipid dropletAutophagyHumansPhosphorylationTyrosineMolecular Biology030304 developmental biology0303 health sciencesMicroscopy ConfocalChemistryCatabolismAutophagyAutophagosomesLipid DropletsImmunohistochemistryCell biologyrab GTP-Binding ProteinsPhosphorylationlipids (amino acids peptides and proteins)RabCRISPR-Cas Systems030217 neurology & neurosurgeryRAB18HeLa CellsJournal of Molecular Biology
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RAB18 impacts autophagy via lipid droplet-derived lipid transfer and is rescued by ATG9A

2018

AbstractAutophagy is a lysosomal degradation pathway that mediates protein and organelle turnover and maintains cellular homeostasis. Autophagosomes transport cargo to lysosomes and their formation is dependent on an appropriate lipid supply. Here, we show that the knockout of the RAB GTPase RAB18 interferes with lipid droplet (LD) metabolism, resulting in an impaired fatty acid mobilization. The reduced LD-derived lipid availability influences autophagy and provokes adaptive modifications of the autophagy network, which include increased ATG2B expression and ATG12-ATG5 conjugate formation as well as enhanced ATG2B and ATG9A phosphorylation. Phosphorylation of ATG9A directs this transmembra…

ChemistryLipid dropletAutophagyOrganellePhosphorylationCellular homeostasisGTPaseRabRAB18Cell biology
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Causes and consequences of DNA damage-induced autophagy.

2021

Abstract Autophagy is a quality control pathway that maintains cellular homeostasis by recycling surplus and dysregulated cell organelles. Identification of selective autophagy receptors demonstrated the existence of pathways that selectively degrade organelles, protein aggregates or pathogens. Interestingly, different types of DNA damage can induce autophagy and autophagy-deficiency leads to genomic instability. Recent studies provided first insights into the pathways that connect autophagy with the DNA damage response. However, the physiological role of autophagy and the identity of its targets after DNA damage remain enigmatic. In this review, we summarize recent literature on the target…

0301 basic medicineGenome instabilityDNA RepairDNA damageAutophagyCellular homeostasisProtein aggregationBiologyGenomic InstabilityCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistry030220 oncology & carcinogenesisOrganelleAutophagyHumansReceptorMolecular BiologyDNADNA DamageMatrix biology : journal of the International Society for Matrix Biology
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