ArticleLife science alliance2025
KANSL3 directs transcriptional programs essential for hepatic metabolism and differentiation.
Article in Life science alliance, 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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Cross-talk between glycosylation pathways: Mechanistic insights and implications for human diseases.Molecular metabolism · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver disease is a leading cause of mortality worldwide. Emerging evidence highlights the significant role of epigenetic regulation in sustaining liver homeostasis, providing new therapeutic strategies for liver disease. Hepatocyte-specific deletion of the epigenetic regulator KANSL3, a key component of the NSL complex, results in early-onset liver disease marked by biliary hyperplasia and hepatic fibrosis. KANSL3 is essential for regulating hepatocyte transcriptional networks important for hepatic steroid and lipid metabolism through histone acetylation. Moreover, single-cell RNA sequencing demonstrated that the loss of KANSL3 disrupts the differentiation of hepatocytes in vivo. The transcriptional programs necessary for hepatocyte differentiation of ductal and fetal liver organoids were severely compromised in the absence of KANSL3. These findings collectively demonstrate a crucial role of the epigenetic regulator KANSL3 in hepatocyte differentiation in liver development and disease.
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