{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["21(12)"],"submitter":["Lim JR"],"pubmed_abstract":["Endoplasmic reticulum (ER) stress is a major contributor to ethanol-induced neurodegeneration. ER-phagy, the selective elimination of specific ER domains, has emerged as a protective mechanism against ER stress. However, its regulation in ethanol-related neurological disorders remains unclear. Here, we investigated the effects and underlying mechanisms of ethanol on ER-phagy in neuronal cells and ethanol-fed mice. Our findings demonstrate that ethanol-induced ER stress is chronically sustained due to impaired ER-phagy. Among ER-phagy receptors, FAM134A expression was notably reduced by ethanol. Ethanol metabolism contributes to the downregulation of SIRT1 activity, leading to increased acetylation of histone H4 lysine 16 (H4K16ac) and enhanced recruitment of bromodomain-containing protein "],"journal":["International journal of biological sciences"],"pagination":["5167-5184"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12435209"],"repository":["biostudies-literature"],"pubmed_title":["Recovery of FAM134A-mediated ER-phagy through BRD4 inhibition alleviates ethanol-induced neurodegeneration."],"pmcid":["PMC12435209"],"pubmed_authors":["Lim JR","Kim SY","Han SJ","Chae CW","Cho JH","Park JY","Kim HJ","Yoon JH","Jung YH","Han HJ","Chang HS"],"additional_accession":[]},"is_claimable":false,"name":"Recovery of FAM134A-mediated ER-phagy through BRD4 inhibition alleviates ethanol-induced neurodegeneration.","description":"Endoplasmic reticulum (ER) stress is a major contributor to ethanol-induced neurodegeneration. ER-phagy, the selective elimination of specific ER domains, has emerged as a protective mechanism against ER stress. However, its regulation in ethanol-related neurological disorders remains unclear. Here, we investigated the effects and underlying mechanisms of ethanol on ER-phagy in neuronal cells and ethanol-fed mice. Our findings demonstrate that ethanol-induced ER stress is chronically sustained due to impaired ER-phagy. Among ER-phagy receptors, FAM134A expression was notably reduced by ethanol. Ethanol metabolism contributes to the downregulation of SIRT1 activity, leading to increased acetylation of histone H4 lysine 16 (H4K16ac) and enhanced recruitment of bromodomain-containing protein ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-01T06:22:29.298Z","creation":"2026-04-08T09:48:33.294Z"},"accession":"S-EPMC12435209","cross_references":{"pubmed":["40959274"],"doi":["10.7150/ijbs.116673"]}}