Structural and functional analyses of APG5 a gene involved in autophagy in yeast
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Cited by (96)
Dual Function of USP14 Deubiquitinase in Cellular Proteasomal Activity and Autophagic Flux
2018, Cell ReportsCitation Excerpt :Further work will be, however, necessary to determine whether there are specific features of the polyubiquitinated substrates and what modulates their susceptibility to proteasomal degradation when autophagy is induced in the cell. To gain further insight into the communication between the UPS and autophagy, we next utilized autophagy-defective ATG5−/− MEFs, where the proper process for autophagic membrane elongation is defective (Kametaka et al., 1996), to examine the overall proteasome activity in the cell. Compared with WT cells, ATG5−/− MEFs showed significantly elevated proteasome activity (Figure 4D), which is consistent with a recent study indicating that pharmacological or genetic inhibition of autophagy results in increased proteasome activity and upregulates proteasomal subunits (Wang et al., 2013).
Horning cell self-digestion: Autophagy wins the 2016 Nobel Prize in Physiology or Medicine
2017, Biomedical JournalAn autophagy gene, HoATG5, is involved in sporulation, cell wall integrity and infection of wounded barley leaves
2016, Microbiological ResearchCitation Excerpt :With the study of molecular basis of autophagy-related genes (ATG) in yeasts, it has now become routine to use genetic approaches to pinpoint precise events in differentiation and development that require the cellular autophagic machinery (Levine and Klionsky, 2004). In Saccharomyces cerevisiae, Atg5 is required for accumulating autophagic bodies in the vacuoles when grown on starvation medium containing phenylmethylsulfonyl fluoride (PMSF), and for surviving in nutrient starving conditions (Kametaka et al., 1996). In Trichoderma reesei, TrAtg5 is involved in the autophagic process, and the TrATG5 deletion mutant is sensitive to starvation conditions, with reduced conidiation and abnormal conidiophores (Liu et al., 2011).
Interplay between sumoylation and phosphorylation for protection against α-synuclein inclusions
2014, Journal of Biological ChemistryCitation Excerpt :PMSF inhibits the activity of numerous vacuolar serine proteases (63) without affecting proteasome function (64). PMSF affects autophagic body formation (65) and leads to accumulation of autophagosomes in the vacuole due to decreased degradation of the autophagic bodies (66). Inhibition of autophagic proteases with PMSF resulted in similar impairment in the clearance of inclusions as with the mutant Δatg1 strain (Fig. 5B).
Role of autophagy in cisplatin resistance in ovarian cancer cells
2014, Journal of Biological ChemistryGlucose starvation inhibits autophagy via vacuolar hydrolysis and induces plasma membrane internalization by down-regulating recycling
2014, Journal of Biological ChemistryCitation Excerpt :We assessed the contributions of endocytosis, endosomal membrane traffic, and autophagy to cell survival during glucose starvation by measuring the viability of strains lacking genes from each pathway. We measured the viability of wild-type cells, cells defective in endocytosis (sla1Δ and rvs161Δ), cells defective in vacuolar protein sorting (vps4Δ), cells defective in autophagy (atg5Δ), and cells defective in vacuolar proteolysis (pep4Δ) after 7 days of starvation (23–26). Wild-type and atg5Δ cells exhibited high viability after 7 days of starvation (Fig. 1A).
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Present address: Department of Life Science, Tokyo Institute of Technology, Nagatsuta 4259, Midori-ku, Yokohama 226, Japan.