Executing cell senescence
Open accessAbstract
Senescence is a permanent form of cell cycle arrest that limits the proliferation of damaged cells and may contribute to tumor suppression and aging. We recently demonstrated that some senescent cell types undergo dramatic changes in chromatin organization that are dependent on the retinoblastoma protein and are associated with the stable repression of some E2F target genes. Here we show how these changes might contribute to the stability of the senescent state.
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Many normal cells senesce when they overexpress certain oncogenes, such as activated components of the RAS-RAF-MEK signaling cascade.
“In addition, many normal cells senesce when they overexpress certain oncogenes, such as activated components of the RAS-RAF-MEK signaling cascade (Bringold and Serrano, 2000; Lundberg et al., 2000; Narita and Lowe, 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Narita and Lowe, 2004
Cells can senesce in response to epigenetic changes to chromatin organization, such as those caused by pharmacological agents or altered expression of proteins that modify DNA or histones.
“Finally, cells can senesce in response to epigenetic changes to chromatin organization—for example, those caused by pharmacological agents or altered expression of proteins that modify DNA or histones (Neumeister et al., 2002; Bandyopadhyay and Medrano, 2003; Narita and Lowe, 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Narita and Lowe, 2004
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- Authors
- Narita, M., & Lowe, S. W.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2004-03
- Volume
- 3
- Issue
- 3
- Pages
- 242-244
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2007093903
- Cited by
- 29
- References
- 17
- Citations by year
- 2026: 1 · 2022: 1 · 2016: 1 · 2015: 2 · 2014: 3 · 2013: 4 · 2012: 4
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- National Cancer Institute (P30CA008748)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, cell cycle arrest, chromatin organization, retinoblastoma protein, E2F target genes, gene repression, tumor suppression, aging
- MeSH terms
- Animals, Chromatin, Humans, Genes, Tumor Suppressor, Retinoblastoma Protein, Cellular Senescence
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