Inducible inactivation of Notch1 causes nodular regenerative hyperplasia in mice

Détails

ID Serval
serval:BIB_3FAD62B6F5FB
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Inducible inactivation of Notch1 causes nodular regenerative hyperplasia in mice
Périodique
Hepatology
Auteur(s)
Croquelois  A., Blindenbacher  A., Terracciano  L., Wang  X., Langer  I., Radtke  F., Heim  M. H.
ISSN
0270-9139 (Print)
Statut éditorial
Publié
Date de publication
03/2005
Volume
41
Numéro
3
Pages
487-96
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar
Résumé
The discovery that the human Jagged1 gene (JAG1) is the Alagille syndrome disease gene indicated that Notch signaling has an important role in bile duct homeostasis. The functional study of this signaling pathway has been difficult because mice with targeted mutations in Jagged1, Notch1, or Notch2 have an embryonic lethal phenotype. We have previously generated mice with inducible Notch1 disruption using an interferon-inducible Cre-recombinase transgene in combination with the loxP flanked Notch1 gene. We used this conditional Notch1 knockout mouse model to investigate the role of Notch1 signaling in liver cell proliferation and differentiation. Deletion of Notch1 did not result in bile duct paucity, but, surprisingly, resulted in a continuous proliferation of hepatocytes. In conclusion, within weeks after Notch1 inactivation, the mice developed nodular regenerative hyperplasia without vascular changes in the liver.
Mots-clé
Animals Calcium-Binding Proteins Cell Proliferation Focal Nodular Hyperplasia/*etiology Hepatectomy Hepatocytes/*pathology Intercellular Signaling Peptides and Proteins *Liver Regeneration Membrane Proteins Mice Mice, Inbred C57BL Proteins/genetics/physiology Signal Transduction/*physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 12:39
Dernière modification de la notice
08/05/2019 17:34
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