PMID:15964995

Citation	Bruggeman, SW, Valk-Lingbeek, ME, van der Stoop, PP, Jacobs, JJ, Kieboom, K, Tanger, E, Hulsman, D, Leung, C, Arsenijevic, Y, Marino, S and van Lohuizen, M (2005) Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice. Genes Dev. 19:1438-43
Abstract	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.
Links	PubMed PMC1151660 Online version:10.1101/gad.1299305
Keywords	Animals; Cell Aging; Cell Differentiation; Cell Proliferation; Cerebellum/cytology; Cyclin-Dependent Kinase Inhibitor p16/deficiency; Cyclin-Dependent Kinase Inhibitor p16/metabolism; Genes, p16; Heterozygote; Lymphoid Tissue/cytology; Mice; Mice, Inbred C57BL; Mice, Knockout; Multipotent Stem Cells/cytology; Multipotent Stem Cells/metabolism; Neurons/cytology; Neurons/metabolism; Nuclear Proteins/deficiency; Nuclear Proteins/genetics; Proto-Oncogene Proteins/deficiency; Proto-Oncogene Proteins/genetics; RNA, Messenger/genetics; RNA, Messenger/metabolism; Repressor Proteins/genetics; Repressor Proteins/metabolism; Tumor Suppressor Protein p14ARF/deficiency; Tumor Suppressor Protein p14ARF/genetics; Tumor Suppressor Protein p14ARF/metabolism
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.