Autophagy is a process whereby cytoplasmic proteins and organelles are sequestered for bulk degradation in the vacuole/lysosome. At present, 16 ATG genes have been found that are essential for autophagosome formation in the yeast Saccharomyces cerevisiae. Most of these genes are also involved in the cytoplasm to vacuole transport pathway, which shares machinery with autophagy. Most Atg proteins are colocalized at the pre-autophagosomal structure (PAS), from which the autophagosome is thought to originate, but the precise mechanism of autophagy remains poorly understood. During a genetic screen aimed to obtain novel gene(s) required for autophagy, we identified a novel ORF, ATG29/YPL166w. atg29Delta cells were sensitive to starvation and induction of autophagy was severely retarded. However, the Cvt pathway operated normally. Therefore, ATG29 is an ATG gene specifically required for autophagy. Additionally, an Atg29-GFP fusion protein was observed to localize to the PAS. From these results, we propose that Atg29 functions in autophagosome formation at the PAS in collaboration with other Atg proteins.
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http://dx.doi.org/10.1016/j.bbrc.2005.10.163 | DOI Listing |
Food Sci Nutr
January 2025
Clinical Medical Research Institute, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang Medical University Urumqi Xinjiang China.
a member of the family, is known for its diverse biological activities, including anti-inflammatory properties. The mechanisms through which polysaccharide (LTP) induces autophagy, however, remain largely unexplored. This study aims to elucidate the role of LTP in autophagy induction and its efficacy in mitigating inflammation within macrophages.
View Article and Find Full Text PDFCell Mol Biol Lett
January 2025
University Cote d'Azur, Inserm, C3M, Nice, France.
Vacuolization of hematopoietic precursors cells is a common future of several otherwise non-related clinical settings such as VEXAS, Chediak-Higashi syndrome and Danon disease. Although these disorders have a priori nothing to do with one other from a clinical point of view, all share abnormal vacuolization in different cell types including cells of the erythroid/myeloid lineage that is likely the consequence of moderate to drastic dysfunctions in the ubiquitin proteasome system and/or the endo-lysosomal pathway. Indeed, the genes affected in these three diseases UBA1, LYST or LAMP2 are known to be direct or indirect regulators of lysosome trafficking and function and/or of different modes of autophagy.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiovascular Medicine, Binzhou Medical University Hospital, 256603 Binzhou, Shandong, China.
Background: Cellular vacuolization is a commonly observed phenomenon under physiological and pathological conditions. However, the mechanisms underlying vacuole formation remain largely unresolved.
Methods: LysoTracker Deep Red probes and Enhanced Green Fluorescent Protein-tagged light chain 3B (LC3B) plasmids were employed to differentiate the types of massive vacuoles.
Int J Mol Sci
January 2025
Division of Renal Medicine, Tungs' Taichung MetroHarbor Hospital, Taichung 433, Taiwan.
Oxidative stress, endoplasmic reticulum (ER) stress, and alterations in autophagy activity have been described as prominent factors mediating many pathological processes in chronic kidney disease (CKD). The accumulation of misfolded proteins in the ER may stimulate the unfolded protein response (UPR). The interplay between autophagy and UPR in hemodialysis (HD) patients remains unclear.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou 730030, China.
The aim of this study was to investigate the inhibitory effect of nintedanib (BIBF) on glioblastoma (GBM) cells and its mechanism of action and to optimize a drug delivery strategy to overcome the limitations posed by the blood-brain barrier (BBB). We analyzed the inhibition of GBM cell lines following BIBF treatment and explored its effect on the autophagy pathway. The cytotoxicity of BIBF was assessed using the CCK-8 assay, and further techniques such as transmission electron microscopy, Western blotting (WB), and flow cytometry were employed to demonstrate that BIBF could block the autophagic pathway by inhibiting the fusion of autophagosomes and lysosomes, ultimately limiting the proliferation of GBM cells.
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