Genes involved in senescence and immortalization
Abstract
Senescence is now understood to be the final phenotypic state adopted by a cell in response to several distinct cell physiological processes, including proliferation, oncogene activation and oxygen free radical toxicity. The role of telomere maintenance in immortalization and the roles of p16(INK4A), p19(ARF), p53 and other genes in senescence are being further elucidated. Significant progress continues to be made in our understanding of cellular senescence and immortalization.
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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 Lundberg et al., 2000
The two senescence pathways are governed by the gatekeeper tumor suppressor proteins p53 and pRB.
“These pathways are governed by the gatekeeper tumor suppressor proteins p53 and pRB (Bringold and Serrano, 2000; Lundberg et al., 2000; Campisi, 2001).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Lundberg et al., 2000
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References 61 · Cited by 313
- Authors
- Lundberg, A. S., Hahn, W. C., Gupta, P., & Weinberg, R. A.
- Affiliations
- Brigham and Women's Hospital (US)
- Whitehead Institute for Biomedical Research (US)
- Corresponding author
- Lundberg, Ante S
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2000-12
- Volume
- 12
- Issue
- 6
- Pages
- 705-709
- ISSN
- 0955-0674 (ISSN-L)
- OpenAlex
- W2041397939
- Cited by
- 313
- References
- 61
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 5 · 2023: 9 · 2022: 4 · 2021: 11 · 2020: 8 · 2019: 7 · 2018: 4 · 2017: 12 · 2016: 5 · 2015: 7 · 2014: 7 · 2013: 9 · 2012: 18
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Cell Biology (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, cell immortalization, telomere maintenance, p16INK4a, p19ARF, p53, oncogene activation, cell proliferation
- MeSH terms
- Animals, Cell Division, Gene Expression Regulation, Humans, Oncogenes, Proteins, Signal Transduction, Telomere, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Genes, p16, Tumor Suppressor Protein p14ARF, Mice
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