Cellular Senescence
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When telomerase is insufficient, cell proliferation causes progressive telomere shortening and eventually replicative senescence as end-protection fails at some short telomeres.
“Cell proliferation in settings of insufficient telomerase results in progressive telomere shortening, ultimately leading to replicative senescence as chromosome end-protection is compromised at a subset of short telomeres (Rodier et al., 2005; Sherr and DePinho, 2000).”
From Short Telomeres and Stem Cell Exhaustion Model Duchenne Muscular Dystrophy in mdx/mTR Mice (2010) · cites this paper as Sherr and DePinho, 2000
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“…same panoply of cell cycle regulatory proteins nortemptation has been to link conclusions drawn from mally associated with arresting cells and undergo “prestudies in these different cell systems, equating senes- mature senescence” (Serrano et al., 1997), whereas escence in mouse and human cells.”
BackgroundExtension of Life-Span by Introduction of Telomerase into Normal Human Cells
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Self-citationTumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
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Self-citationMyc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
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“Removing the telomerements TERT reconstitution in the immortalization pro- cess (Kiyono et al., 1998).”
Backgroundp53- and ATM-Dependent Apoptosis Induced by Telomeres Lacking TRF2
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“On the other hand, observations that late-generation mTR null cells mTR null animals, the levels of p53 and p53-responsive with shortened telomeres (Chin et al., 1999) or cells with otherwise disrupted telomere structures (Karlseder et al., 1999) initiate p53-dependent DNA damage responses lend…”
BackgroundSelf-citationDevelopmental and tissue-specific regulation of mouse telomerase and telomere length.
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- Authors
- Sherr, C. J., & DePinho, R. A.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Harvard University (US)
- Corresponding author
- Sherr, Charles J
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2000-08
- Volume
- 102
- Issue
- 4
- Pages
- 407-410
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2324248025
- Cited by
- 745
- References
- 20
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 13 · 2023: 10 · 2022: 13 · 2021: 19 · 2020: 20 · 2019: 16 · 2018: 7 · 2017: 30 · 2016: 17 · 2015: 19 · 2014: 24 · 2013: 19 · 2012: 31
- FWCI
- 36.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, biological aging, human fibroblasts, mouse fibroblasts, culture shock, telomere integrity, cell cycle inhibitors, oncogenic transformation, chromosome stability
- MeSH terms
- Animals, Humans, Mitosis, Models, Biological, Telomere, Cellular Senescence
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