ArticleAlcoholism, clinical and experimental research2016
Study of Ethanol-Induced Golgi Disorganization Reveals the Potential Mechanism of Alcohol-Impaired N-Glycosylation.
Article in Alcoholism, clinical and experimental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Alcohol-induced altered glycans in human tracheal epithelial cells promote bacterial adhesion.FEBS open bio · 2026Article
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- Alcohol induces α2-6sialo mucin O-glycans that kill U937 macrophages mediated by sialic acid-binding immunoglobulin-like lectin 7 (Siglec 7).FEBS open bio · 2025Article
- Alcohol-induced Golgiphagy is triggered by the downregulation of Golgi GTPase RAB3D.Autophagy · 2024Article
- Diagnostic Usefulness of Disialotransferrin as an Indicator of Binge Drinking in Children and Adolescents.Journal of clinical medicine · 2024Article
- Zonal expression of StARD1 and oxidative stress in alcoholic-related liver disease.Journal of lipid research · 2023Article
- Intracellular traffic and polarity in brain development.Frontiers in neuroscience · 2023Review
- Alcohol and Prostate Cancer: Time to Draw Conclusions.Biomolecules · 2022Review
- Changes in SerumBiomolecules · 2022Article
- Alcohol-Induced Liver Injury: Down-regulation and Redistribution of Rab3D Results in Atypical Protein Trafficking.Hepatology communications · 2022Article
- Construction of long non-coding RNA- and microRNA-mediated competing endogenous RNA networks in alcohol-related esophageal cancer.PloS one · 2022Article
- TNF-α/NF-κB signaling epigenetically represses PSD4 transcription to promote alcohol-related hepatocellular carcinoma progression.Cancer medicine · 2021Article
- Article
- Unlocking Golgi: Why Does Morphology Matter?Biochemistry. Biokhimiia · 2019Review
- The Role of Alcohol-Induced Golgi Fragmentation for Androgen Receptor Signaling in Prostate Cancer.Molecular cancer research : MCR · 2019Article
- Giantin Is Required for Post-Alcohol Recovery of Golgi in Liver Cells.Biomolecules · 2018Article
- THE IMPACT OF ALCOHOL ON PRO-METASTATIC N-GLYCOSYLATION IN PROSTATE CANCER.Krimskii zhurnal eksperimental'noi i klinicheskoi meditsiny = Kryms'kyi zhurnal eksperymental'noi ta klinichnoi medytsyny = Crimean journal of experimental and clinical medicine · 2018Article
- Pathogenesis of Alcohol-Associated Liver Disease.Journal of clinical and experimental hepatologyReview
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4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIt is known that ethanol (EtOH) and its metabolites have a negative effect on protein glycosylation. The fragmentation of the Golgi apparatus induced by alteration of the structure of largest Golgi matrix protein, giantin, is the major consequence of damaging effects of EtOH-metabolism on the Golgi; however, the link between this and abnormal glycosylation remains unknown. Because previously we have shown that Golgi morphology dictates glycosylation, we examined the effect EtOH administration has on function of Golgi residential enzymes involved in N-glycosylation.
methodsHepG2 cells transfected with mouse ADH1 (VA-13 cells) were treated with 35 mM EtOH for 72 hours. Male Wistar rats were pair-fed Lieber-DeCarli diets for 5 to 8 weeks. Characterization of Golgi-associated mannosyl (α-1,3-)-glycoprotein beta-1,2-N-acetylglucosaminyltransferase (MGAT1), α-1,2-mannosidase (Man-I), and α-mannosidase II (Man-II) were performed in VA-13 cells and rat hepatocytes followed by three-dimensional structured illumination microscopy (3D SIM).
resultsFirst, we detected that EtOH administration results in the loss of sialylated N-glycans on asialoglycoprotein receptor; however, the high-mannose-type N-glycans are increased. Further analysis by 3D SIM revealed that EtOH treatment despite Golgi disorganization does not change cis-Golgi localization for Man-I, but does induce medial-to-cis relocation of MGAT1 and Man-II. Using different approaches, including electron microscopy, we revealed that EtOH treatment results in dysfunction of ADP-ribosylation factor 1 (Arf1) GTPase followed by a deficiency in COPI vesicles at the Golgi. Silencing beta-COP or expression of GDP-bound mutant Arf1(T31N) mimics the EtOH effect on retaining MGAT1 and Man-II at the cis-Golgi, suggesting that (i) EtOH specifically blocks activation of Arf1, and (ii) EtOH alters the proper localization of Golgi enzymes through impairment of COPI. Importantly, the level of MGAT1 was reduced, because likely MGAT1, contrary to Man-I and Man-II, is giantin sensitive.
conclusionsThus, we provide the mechanism by which EtOH-induced Golgi remodeling may significantly modify formation of N-glycans.
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