The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways
Open accessAbstract
Bmi-1 is required for the post-natal maintenance of stem cells in multiple tissues including the central nervous system (CNS) and peripheral nervous system (PNS). Deletion of Ink4a or Arf from Bmi-1-/- mice partially rescued stem cell self-renewal and stem cell frequency in the CNS and PNS, as well as forebrain proliferation and gut neurogenesis. Arf deficiency, but not Ink4a deficiency, partially rescued cerebellum development, demonstrating regional differences in the sensitivity of progenitors to p16 Ink4a and p19 Arf. Deletion of both Ink4a and Arf did not affect the growth or survival of Bmi-1-/- mice or completely rescue neural development. Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a and Arf, but additional pathways must also function downstream of Bmi-1.
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Cites
Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.
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Self-citationJacobs, J. J. L., Kieboom, K., Marino, S., DePinho, R. A., & van Lohuizen, M. (1999) · Nature · doi:10.1038/16476 · Cited by 1,580
Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
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Bmi-1 determines the proliferative capacity of normal and leukaemic stem cells.
Lessard, J., & Sauvageau, G. (2003) · Nature · doi:10.1038/nature01572 · Cited by 1,452
Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis
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Tumor suppression by Ink4a-Arf: progress and puzzles.
Lowe, S. W., & Sherr, C. J. (2003) · Current Opinion in Genetics & Development · doi:10.1016/s0959-437x(02)00013-8 · Cited by 699 · cited 4×
“Rb activation, changes in p21 cip1 expression affect the levels of p16 Ink4a that are required to inhibit proliferation (Lowe and Sherr 2003).”
BackgroundInfluentialControl of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1
Itahana, K., Zou, Y., Itahana, Y., Martinez, J.-L., Beausejour, C., Jacobs, J. J. L., van Lohuizen, M., Band, V., Campisi, J., & Dimri, G. P. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.1.389-401.2003 · Cited by 438
Cited by
Cancer stem cells in solid tumours: accumulating evidence and unresolved questions
Visvader, J. E., & Lindeman, G. J. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2499 · Cited by 3,429
Mechanisms and Functional Implications of Adult Neurogenesis
Zhao, C., Deng, W., & Gage, F. H. (2008) · Cell · doi:10.1016/j.cell.2008.01.033 · Cited by 3,007
Cancer stem cells: an old idea–a paradigm shift
Wicha, M. S., Liu, S., & Dontu, G. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-3153 · Cited by 1,378
Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells
Yilmaz, Ö. H., Valdez, R., Theisen, B. K., Guo, W., Ferguson, D. O., Wu, H., & Morrison, S. J. (2006) · Nature · doi:10.1038/nature04703 · Cited by 1,113
Self-citationClement, V., Sanchez, P., de Tribolet, N., Radovanovic, I., & Ruiz i Altaba, A. (2007) · Current Biology · doi:10.1016/j.cub.2006.11.033 · Cited by 1,050
Metadata
- Authors
- Molofsky, A. V., He, S., Bydon, M., Morrison, S. J., & Pardal, R.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2005-06-15
- Volume
- 19
- Issue
- 12
- Pages
- 1432-1437
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2080790343
- Cited by
- 588
- References
- 7
- Type
- posted content
- Language
- en
- Open access
- diamond
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- CoChat. (2026). Citation check: Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways. https://app.cochat.ai/papers/10.1101/gad.1299505
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- Molofsky, A. V., He, S., Bydon, M., Morrison, S. J., & Pardal, R. (2005). Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways. Genes & Development. https://doi.org/10.1101/gad.1299505
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