The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
CCAAT enhancer- binding protein beta is required for normal hepatocyte proliferation in mice after partial hepatectomy.
Open accessAbstract
After two-thirds hepatectomy, normally quiescent liver cells are stimulated to reenter the cell cycle and proliferate to restore the original liver mass. The level of bZIP transcription factor CCAAT enhancer-binding protein beta (C/EBPbeta) increases in the liver during the period of cell proliferation. The significance of this change in C/EBP expression is not understood. To determine the role of C/EBPbeta in the regenerating liver, we examined the regenerative response after partial hepatectomy in mice that contain a targeted disruption of the C/EBPbeta gene. Posthepatectomy, hepatocyte DNA synthesis was decreased to 25% of normal in C/EBPbeta -/- mice. The reduced regenerative response was associated with a prolonged period of hypoglycemia that was independent of expression of C/EBPalpha protein and gluconeogenic genes. C/EBPbeta -/- livers showed reduced expression of immediate-early growth-control genes including the Egr-1 transcription factor, mitogen-activated protein kinase protein tyrosine phosphatase (MKP-1), and HRS, a delayed-early gene that encodes an mRNA splicing protein. Cyclin B and E gene expression were dramatically reduced in C/EBPbeta -/- livers whereas cyclin D1 expression was normal. The abnormalities in immediate-early gene expression in C/EBPbeta -/- livers were distinct from those seen in IL-6 -/- livers. These data link C/EBPbeta to the activation of metabolic and growth response pathways in the regenerating liver and demonstrate that C/EBPbeta is required for a normal proliferative response.
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“Regaining liver mass despite deficient DNA synthesis is a general phenomenon in animal models that are defective in liver regeneration, which most likely results from hypertrophy of hepatocytes despite G1/S arrest (3”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [18]
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Self-citationA nuclear factor for IL‐6 expression (NF‐IL6) is a member of a C/EBP family.
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Liver regeneration: from myth to mechanism
Taub, R. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1489 · Cited by 1,567
Self-citationCCAAT/enhancer-binding proteins: structure, function and regulation
Ramji, D. P., & Foka, P. (2002) · Biochemical Journal · doi:10.1042/bj20020508 · Cited by 1,404
Fausto, N. (2000) · Journal of Hepatology · doi:10.1016/s0168-8278(00)80412-2 · Cited by 1,022
Inductive angiocrine signals from sinusoidal endothelium are required for liver regeneration
Ding, B., Nolan, D. J., Butler, J. M., James, D., Babazadeh, A. O., Rosenwaks, Z., Mittal, V., Kobayashi, H., Shido, K., Lyden, D. C., et al. (2010) · Nature · doi:10.1038/nature09493 · Cited by 853
Met provides essential signals for liver regeneration
Borowiak, M., Garratt, A. N., Wüstefeld, T., Strehle, M., Trautwein, C., & Birchmeier, C. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0403412101 · Cited by 497
Metadata
- Authors
- Greenbaum, L. E., Li, W., Cressman, D. E., Peng, Y., Ciliberto, G., Poli, V, & Taub, R.
- Affiliations
- University of Pennsylvania (US)
- Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" (IT)
- University of Dundee (GB)
- Venue
- Journal of Clinical Investigation
- Published
- 1998-09-01
- Volume
- 102
- Issue
- 5
- Pages
- 996-1007
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC508965
- OpenAlex
- W2055209830
- Cited by
- 270
- References
- 72
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 10 · 2022: 5 · 2021: 8 · 2020: 5 · 2019: 3 · 2018: 7 · 2017: 6 · 2016: 3 · 2015: 8 · 2014: 6 · 2013: 7 · 2012: 5
- FWCI
- 12.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Funders
- National Institutes of Health (K08 DK, 5r01dk049629-05)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044237, DK 44237, DK-49629, P01DK049210, DK 49210)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
- Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
- Keywords
- C/EBPβ, hepatocyte proliferation, liver regeneration, partial hepatectomy, knockout mice, hypoglycemia, immediate early genes, EGR1, MKP-1, Hrs, cyclin B, cyclin E, cyclin D1, bZIP transcription factors, DNA synthesis
- MeSH terms
- Animals, Cell Division, Cells, Cultured, DNA, DNA-Binding Proteins, Gene Expression Regulation, Gluconeogenesis, Hepatectomy, Immunohistochemistry, Liver Regeneration, Nuclear Proteins, Phosphoproteins, RNA Splicing, RNA, Messenger, Transcription Factors, Trans-Activators, S Phase, Cyclins, Mice, Knockout, CCAAT-Enhancer-Binding Proteins, STAT3 Transcription Factor, Mice, Endosomal Sorting Complexes Required for Transport
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