Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice
Détails
ID Serval
serval:BIB_D109E221B117
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice
Périodique
Genes and Development
ISSN
0890-9369 (Print)
Statut éditorial
Publié
Date de publication
06/2005
Volume
19
Numéro
12
Pages
1438-43
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jun 15
Research Support, Non-U.S. Gov't --- Old month value: Jun 15
Résumé
The Polycomb group (PcG) gene Bmi1 promotes cell proliferation and stem cell self-renewal by repressing the Ink4a/Arf locus. We used a genetic approach to investigate whether Ink4a or Arf is more critical for relaying Bmi1 function in lymphoid cells, neural progenitors, and neural stem cells. We show that Arf is a general target of Bmi1, however particularly in neural stem cells, derepression of Ink4a contributes to Bmi1(-/-) phenotypes. Additionally, we demonstrate haploinsufficient effects for the Ink4a/Arf locus downstream of Bmi1 in vivo. This suggests differential, cell type-specific roles for Ink4a versus Arf in PcG-mediated (stem) cell cycle control.
Mots-clé
Animals
Cell Aging
Cell Differentiation
Cell Proliferation
Cerebellum/cytology
Cyclin-Dependent Kinase Inhibitor p16/deficiency/metabolism
*Genes, p16
Heterozygote
Lymphoid Tissue/cytology
Mice
Mice, Inbred C57BL
Mice, Knockout
Multipotent Stem Cells/*cytology/*metabolism
Neurons/*cytology/*metabolism
Nuclear Proteins/*deficiency/genetics
Proto-Oncogene Proteins/*deficiency/genetics
RNA, Messenger/genetics/metabolism
Repressor Proteins/genetics/metabolism
Tumor Suppressor Protein p14ARF/deficiency/*genetics/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 13:31
Dernière modification de la notice
20/08/2019 16:51