ArticleJournal of molecular cell biology2026
Emerging role of FUS in TGFB1 and COL1A1 transcription dependent on GADD45B to induce NASH-fibrosis.
Article in Journal of molecular cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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11 authors.
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Abstract
Fused in sarcoma (FUS), a DNA-RNA binding protein, affects gene transcription, while its role in non-alcoholic steatohepatitis (NASH)-fibrosis is not well understood. In this study, immunohistochemistry and western blot analysis were used to detect the expression of FUS in liver samples from patients with NASH and in LX-2 cells. Immunofluorescence staining showed that FUS co-localized with growth arrest and DNA damage 45β (GADD45B) in hepatic stellate cells (HSCs). Chromatin immunoprecipitation combined with quantitative PCR and luciferase reporter assays were performed to validate the binding sites and transcriptional activity of FUS to the TGFB1 and COL1A1 promoters. Gadd45b knockout (Gadd45b KO) and wild-type mice with the NASH-fibrosis model validated the role of GADD45B in NASH-fibrosis. Downregulation of GADD45B reduced HSC activation triggered by TGFB1 stimulation or FUS overexpression. Ameliorated collagen deposition and decreased nuclear FUS content in HSCs were detected in Gadd45b KO mice. Overall, this study suggests that FUS and GADD45B could be potential treatment targets for NASH-fibrosis.
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