Regulation of the G1/S Transition in Hepatocytes: Involvement of the Cyclin-Dependent Kinase Cdk1 in the DNA Replication

Anne Corlu 1 Pascal Loyer 1, *
* Auteur correspondant
Abstract : A singular feature of adult differentiated hepatocytes is their capacity to proliferate allowing liver regeneration. This review emphasizes the literature published over the last 20 years that established the most important pathways regulating the hepatocyte cell cycle. Our article also aimed at illustrating that many discoveries in this field benefited from the combined use of in vivo models of liver regeneration and in vitro models of primary cultures of human and rodent hepatocytes. Using these models, our laboratory has contributed to decipher the different steps of the progression into the G1 phase and the commitment to S phase of proliferating hepatocytes. We identified the mitogen dependent restriction point located at the two-thirds of the G1 phase and the concomitant expression and activation of both Cdk1 and Cdk2 at the G1/S transition. Furthermore, we demonstrated that these two Cdks contribute to the DNA replication. Finally, we provided strong evidences that Cdk1 expression and activation is correlated to extracellular matrix degradation upon stimulation by the pro-inflammatory cytokine TNFα leading to the identification of a new signaling pathway regulating Cdk1 expression at the G1/S transition. It also further confirms the well-orchestrated regulation of liver regeneration via multiple extracellular signals and pathways.
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Article dans une revue
International Journal of Hepatology, 2012, 2012, pp.689324. 〈10.1155/2012/689324〉
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http://www.hal.inserm.fr/inserm-00864116
Contributeur : Morgane Le Corre <>
Soumis le : vendredi 20 septembre 2013 - 13:33:16
Dernière modification le : mercredi 16 mai 2018 - 11:23:30

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Anne Corlu, Pascal Loyer. Regulation of the G1/S Transition in Hepatocytes: Involvement of the Cyclin-Dependent Kinase Cdk1 in the DNA Replication. International Journal of Hepatology, 2012, 2012, pp.689324. 〈10.1155/2012/689324〉. 〈inserm-00864116〉

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