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Knockdown of FAF2 Prevents Alcohol-Induced Steatosis in Mouse Liver

GSE270659 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/02/26 Platform GPL24247
Summary
Alcohol is metabolized in the liver, and chronic consumption can lead to inflammation, scarring, and damage to liver cells. The pathogenesis of alcoholic liver disease (ALD), a complicated condition, is characterized by a succession of histopathological alterations that occur through a multistep and multifactorial process. FAF2/UBXD8/ETEA is a ubiquitin ligase adaptor protein and plays a crucial role in the ubiquitin-mediated degradation of misfolded proteins in the endoplasmic reticulum. Recent GWAS study indicated that FAF2 was associated with ALD, but the exact function of FAF2 in ALD has not been identified yet. The objective of this study was to investigate the role of FAF2 in ALD.Our study revealed a noteworthy rise in hepatic FAF2 protein expression among individuals with ALD and mice subjected to chronic-plus-single binge ethanol feeding. The suppression of FAF2 in mice liver provided protection against alcohol-induced hepatic steatosis.
Published in
Silencing FAF2 mitigates alcohol-induced hepatic steatosis by modulating lipolysis and PCSK9 pathway
Huda N, Kusumanchi P, Jiang Y et al. · Hepatology communications 2025 · PMID 39969435 · doi:10.1097/HC9.0000000000000641
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Also filed as BioProject PRJNA1127643 and SRA study SRP515752. Searching any of these in the dataset finder brings you back here.

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