ArticleScientific reports2015
CCAAT/enhancer-binding protein α is required for hepatic outgrowth via the p53 pathway in zebrafish.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Functional Characterization of Trypsin in the Induction of Biologically Live Bait Feeding in Mandarin Fish (Cells · 2025Article
- A review of C/EBP α: a potential novel target for solid tumor intervention.Journal of translational medicine · 2025Review
- Molecular Genealogy of Metabolic-associated Hepatocellular Carcinoma.Seminars in liver disease · 2024Review
- Aquaporin 8ab is required in zebrafish embryonic intestine development.Acta biochimica et biophysica Sinica · 2022Article
- An Epigenetic Switch Between Differentiation and Proliferation in Hepatoblastoma.Cellular and molecular gastroenterology and hepatology · 2021Article
- Zebrafish Cancer Predisposition Models.Frontiers in cell and developmental biology · 2021Review
- PIWIL3/OIP5-AS1/miR-367-3p/CEBPA feedback loop regulates the biological behavior of glioma cells.Theranostics · 2018Article
- Dose-dependent effects of gamma radiation on the early zebrafish development and gene expression.PloS one · 2017Article
- Making It New Again: Insight Into Liver Development, Regeneration, and Disease From Zebrafish Research.Current topics in developmental biology · 2017Review
- Role of C/EBP-α in Adriamycin-induced podocyte injury.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCAAT/enhancer-binding protein α (C/ebpα) is a transcription factor that plays important roles in the regulation of hepatogenesis, adipogenesis and hematopoiesis. Disruption of the C/EBPα gene in mice leads to disturbed liver architecture and neonatal death due to hypoglycemia. However, the precise stages of liver development affected by C/ebpα loss are poorly studied. Using the zebrafish embryo as a model organism, we show that inactivation of the cebpa gene by TALENs results in a small liver phenotype. Further studies reveal that C/ebpα is distinctively required for hepatic outgrowth but not for hepatoblast specification. Lack of C/ebpα leads to enhanced hepatic cell proliferation and subsequent increased cell apoptosis. Additional loss of p53 can largely rescue the hepatic defect in cebpa mutants, suggesting that C/ebpα plays a role in liver growth regulation via the p53 pathway. Thus, our findings for the first time demonstrate a stage-specific role for C/ebpα during liver organogenesis.
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Registered trials
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