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Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver.
- Source :
- EMBO Journal; 4/1/2002, Vol. 21 Issue 7, p1782-1790, 9p
- Publication Year :
- 2002
-
Abstract
- Mice lacking the AP-1 transcription factor c-jun die at mid-gestation showing heart defects and impaired hepatogenesis. To inactivate c-jun in hepatocytes, mice carrying a floxed c-jun allele were generated. Perinatal liver-specific c-jun deletion caused reduced hepatocyte proliferation and decreased body size. After partial hepatectomy, half of the mutants died and liver regeneration was impaired. This phenotype was not present in mice lacking the N-terminal phosphorylation sites of c-Jun. The failure to regenerate was accompanied by increased cell death and lipid accumulation in hepatocytes. Moreover, cyclindependent kinases and several cell cycle regulators were affected, resulting in inefficient G<subscript>1</subscript>-S phase progression. These studies identify c-Jun as a critical regulator of hepatocyte proliferation and survival during liver development and regeneration. [ABSTRACT FROM AUTHOR]
- Subjects :
- LIVER cells
CELL proliferation
MICE
TRANSCRIPTION factors
PREGNANCY
HEPATECTOMY
Subjects
Details
- Language :
- English
- ISSN :
- 02614189
- Volume :
- 21
- Issue :
- 7
- Database :
- Complementary Index
- Journal :
- EMBO Journal
- Publication Type :
- Academic Journal
- Accession number :
- 12955761
- Full Text :
- https://doi.org/10.1093/emboj/21.7.1782