ArticleCell cycle (Georgetown, Tex.)2012
Loss of a membrane trafficking protein αSNAP induces non-canonical autophagy in human epithelia.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- A pathogenic mutation in α-SNAP impairs membrane lipid binding by concealing a critical hydrophobic loop.Communications biology · 2026Article
- Article
- Alpha-SNAP (M105I) mutation promotes neuronal differentiation of neural stem/progenitor cells through overactivation of AMPK.Frontiers in cell and developmental biology · 2023Article
- Review
- SON DNA-binding protein mediates macrophage autophagy and responses to intracellular infection.FEBS letters · 2020Article
- Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- A miRNA screen procedure identifiesF1000Research · 2020Article
- Article
- Pleiotropic effects of alpha-SNAP M105I mutation on oocyte biology: ultrastructural and cellular changes that adversely affect female fertility in mice.Scientific reports · 2019Article
- Imbalance of autophagy and apoptosis in intestinal epithelium lacking the vitamin D receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- THANATOS: an integrative data resource of proteins and post-translational modifications in the regulation of autophagy.Autophagy · 2018Article
- A membrane fusion protein, Ykt6, regulates epithelial cell migration via microRNA-mediated suppression of Junctional Adhesion Molecule A.Cell cycle (Georgetown, Tex.) · 2018Article
- Stall in Canonical Autophagy-Lysosome Pathways Prompts Nucleophagy-Based Nuclear Breakdown in Neurodegeneration.Current biology : CB · 2017Article
- SNARE priming is essential for maturation of autophagosomes but not for their formation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Shear stress induces noncanonical autophagy in intestinal epithelial monolayers.Molecular biology of the cell · 2017Article
- α-SNAP is expressed in mouse ovarian granulosa cells and plays a key role in folliculogenesis and female fertility.Scientific reports · 2017Article
- A vesicle trafficking protein αSNAP regulates Paneth cell differentiation in vivo.Biochemical and biophysical research communications · 2017Article
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4 authors at 3 institutions in 2 countries.
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Abstract
Autophagy is a catabolic process that sequesters intracellular proteins and organelles within membrane vesicles called autophagosomes with their subsequent delivery to lyzosomes for degradation. This process involves multiple fusions of autophagosomal membranes with different vesicular compartments; however, the role of vesicle fusion in autophagosomal biogenesis remains poorly understood. This study addresses the role of a key vesicle fusion regulator, soluble N-ethylmaleimide-sensitive factor attachment protein α (αSNAP), in autophagy. Small interfering RNA-mediated downregulation of αSNAP expression in cultured epithelial cells stimulated the autophagic flux, which was manifested by increased conjugation of microtubule-associated protein light chain 3 (LC3-II) and accumulation of LC3-positive autophagosomes. This enhanced autophagy developed via a non-canonical mechanism that did not require beclin1-p150-dependent nucleation, but involved Atg5 and Atg7-mediated elongation of autophagosomal membranes. Induction of autophagy in αSNAP-depleted cells was accompanied by decreased mTOR signaling but appeared to be independent of αSNAP-binding partners, N-ethylmaleimide-sensitive factor and BNIP1. Loss of αSNAP caused fragmentation of the Golgi and downregulation of the Golgi-specific GTP exchange factors, GBF1, BIG1 and BIG2. Pharmacological disruption of the Golgi and genetic inhibition of GBF1 recreated the effects of αSNAP depletion on the autophagic flux. Our study revealed a novel role for αSNAP as a negative regulator of autophagy that acts by enhancing mTOR signaling and regulating the integrity of the Golgi complex.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.