Cited by 495Telomeres, Telomerase, and SenescenceHematopoietic Stem Cell TransplantationGenetics, Aging, and Longevity in Model Organisms

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Bmi1, stem cells, and senescence regulation

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Park, In-Kyung, Morrison, Sean J., Clarke, Michael F.·2004·Journal of Clinical Investigation

DOI 10.1172/jci200420800PMC PMC311443

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Abstract

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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Authors: Park, I.-K., Morrison, S. J., & Clarke, M. F.
Affiliations: University of Michigan (US)
ORCID: Park, In-Kyung
Morrison, Sean J.
Clarke, Michael F.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2004-01-15
Volume: 113
Issue: 2
Pages: 175-179
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci200420800
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: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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