Research ExplorerPublicationsImpaired postnatal hepatocyte proliferation and liver regene...

Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver

Standard

Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver. / Behrens, Axel; Sibilia, Maria; David, Jean-Pierre; Möhle-Steinlein, Uta; Tronche, François; Schütz, Günther; Wagner, Erwin F.

In: EMBO J, Vol. 21, No. 7, 02.04.2002, p. 1782-90.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Behrens, A, Sibilia, M, David, J-P, Möhle-Steinlein, U, Tronche, F, Schütz, G & Wagner, EF 2002, 'Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver', EMBO J, vol. 21, no. 7, pp. 1782-90. https://doi.org/10.1093/emboj/21.7.1782

APA

Behrens, A., Sibilia, M., David, J-P., Möhle-Steinlein, U., Tronche, F., Schütz, G., & Wagner, E. F. (2002). Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver. EMBO J, 21(7), 1782-90. https://doi.org/10.1093/emboj/21.7.1782

Vancouver

Behrens A, Sibilia M, David J-P, Möhle-Steinlein U, Tronche F, Schütz G et al. Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver. EMBO J. 2002 Apr 2;21(7):1782-90. https://doi.org/10.1093/emboj/21.7.1782

Bibtex

@article{31a37ccc8307489eb8aabb9d22039816,
title = "Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver",
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, cyclin-dependent kinases and several cell cycle regulators were affected, resulting in inefficient G(1)-S phase progression. These studies identify c-Jun as a critical regulator of hepatocyte proliferation and survival during liver development and regeneration.",
keywords = "Animals, Cell Cycle, Cell Division, Female, Hepatocytes, Liver, Liver Regeneration, Male, Mice, Mice, Inbred C57BL, Mutagenesis, Proto-Oncogene Proteins c-jun",
author = "Axel Behrens and Maria Sibilia and Jean-Pierre David and Uta M{\"o}hle-Steinlein and Fran{\c c}ois Tronche and G{\"u}nther Sch{\"u}tz and Wagner, {Erwin F}",
year = "2002",
month = apr,
day = "2",
doi = "10.1093/emboj/21.7.1782",
language = "English",
volume = "21",
pages = "1782--90",
journal = "EMBO J",
issn = "0261-4189",
publisher = "NATURE PUBLISHING GROUP",
number = "7",

}

RIS

TY - JOUR

T1 - Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liver

AU - Behrens, Axel

AU - Sibilia, Maria

AU - David, Jean-Pierre

AU - Möhle-Steinlein, Uta

AU - Tronche, François

AU - Schütz, Günther

AU - Wagner, Erwin F

PY - 2002/4/2

Y1 - 2002/4/2

N2 - 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, cyclin-dependent kinases and several cell cycle regulators were affected, resulting in inefficient G(1)-S phase progression. These studies identify c-Jun as a critical regulator of hepatocyte proliferation and survival during liver development and regeneration.

AB - 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, cyclin-dependent kinases and several cell cycle regulators were affected, resulting in inefficient G(1)-S phase progression. These studies identify c-Jun as a critical regulator of hepatocyte proliferation and survival during liver development and regeneration.

KW - Animals

KW - Cell Cycle

KW - Cell Division

KW - Female

KW - Hepatocytes

KW - Liver

KW - Liver Regeneration

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mutagenesis

KW - Proto-Oncogene Proteins c-jun

U2 - 10.1093/emboj/21.7.1782

DO - 10.1093/emboj/21.7.1782

M3 - SCORING: Journal article

C2 - 11927562

VL - 21

SP - 1782

EP - 1790

JO - EMBO J

JF - EMBO J

SN - 0261-4189

IS - 7

ER -