Bmi1, stem cells, and senescence regulation
Open accessAbstract
Stem cells generate the differentiated cell types within many organs throughout the lifespan of an organism and are thus ultimately responsible for the longevity of multicellular organisms.Therefore, senescence of stem cells must be prevented.Bmi1 is required for the maintenance of adult stem cells in some tissues partly because it represses genes that induce cellular senescence and cell death.
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Many adult stem or progenitor cells do not proliferate indefinitely, whether mouse or human in origin.
“However, many adult stem or progenitor cells do not proliferate indefinitely, whether mouse or human in origin (Geiger and Van Zant, 2002; Chen, 2004; Park et al., 2004; Villa et al., 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Park et al., 2004
The 'Stem cells and senescence' section says mouse hematopoietic stem cells can undergo only a limited number of serial transplants, suggesting they may not be immortal. It does not establish the same limit for human adult stem or progenitor cells, or for many cell types generally; the 'Future directions' section also notes that stem-cell senescence during normal aging is controversial. No page numbers were available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredPolycomb group proteins play a role in regulation of expression from the Ink4a/Arf locus, and Bmi1 is implicated in this process.
“Several studies suggest a role for polycomb group proteins in the regulation of expression from the Ink4a/Arf locus, and Bmi1, a key component of the polycomb complex, has been widely implicated in this process (37,38).”
From Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration in Mice (2009) · cites this paper as [37]
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- Authors
- Park, I.-K., Morrison, S. J., & Clarke, M. F.
- Affiliations
- University of Michigan (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2004-01-15
- Volume
- 113
- Issue
- 2
- Pages
- 175-179
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC311443
- OpenAlex
- W2104666653
- Cited by
- 495
- References
- 59
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 7 · 2023: 13 · 2022: 19 · 2021: 20 · 2020: 17 · 2019: 17 · 2018: 19 · 2017: 24 · 2016: 37 · 2015: 33 · 2014: 20 · 2013: 37 · 2012: 30
- FWCI
- 15.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- BMI1, stem cells, cellular senescence, stem cell maintenance, longevity, cell death, gene repression
- MeSH terms
- Animals, Cell Line, Gene Expression Regulation, Humans, Models, Biological, Mutation, Nuclear Proteins, Proto-Oncogene Proteins, Repressor Proteins, Stem Cells, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Protein p14ARF, Mice, Polycomb Repressive Complex 1
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