ArticleScientific reports2025
HCF-1 as a key modulator of OGT function and O-GlcNAcylation in the liver.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Hcfc1 and Ogt Mediate Zebrafish CNS Regeneration Through Hippo/Yap Signalling.Cell proliferation · 2026Article
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host cell factor-1 (HCF-1) is a transcriptional coregulator essential for maintaining liver function and cellular metabolism. O-linked N-acetylglucosamine transferase (OGT) is a key nutrient-sensing enzyme that catalyzes protein O-GlcNAcylation, a critical post-translational modification regulating metabolic pathways. This study investigates the role of hepatocyte-specific depletion of HCF-1 in regulating OGT stability, activity, and cellular localization in hepatocytes. Using a transgenic mouse model with hepatocyte-specific HCF-1 deletion, we assessed the impact of HCF-1 loss on OGT expression and O-GlcNAcylation activity. OGT protein levels, mRNA expression, and cellular localization were evaluated using molecular and histological techniques. Comparisons were made with control mice and hepatocytes under nutrient-starved conditions. Hepatocyte-specific HCF-1 deletion led to progressive loss of HCF-1 protein and a concomitant decrease in OGT levels and global O-GlcNAcylation. Loss of HCF-1 did not alter OGT mRNA levels, suggesting post-translational regulation. Immunofluorescence revealed reduced nuclear OGT and O-GlcNAcylation, mimicking changes observed under fasting conditions. Isolated HCF-1-deficient hepatocytes showed impaired adhesion, further underscoring HCF-1's role in hepatocyte function. Notably, in heterozygous Hcfc1
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