The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Radiation-induced cell cycle arrest compromised by p21 deficiency
Abstract
The protein p21 is a dual inhibitor of cyclin-dependent kinases and proliferating-cell nuclear antigen (PCNA), both of which are required for passage through the cell cycle. The p21 gene is under the transcriptional control of p53 (ref. 5), suggesting that p21 might promote p53-dependent cell cycle arrest or apoptosis. p21 has also been implicated in cell senescence and in cell-cycle withdrawal upon terminal differentiation. Here we investigate the role of p21 in these processes using chimaeric mice composed partly of p21-/- and partly of p21+/+ cells. Immunohistochemical studies of the p21+/+ and p21-/- components of adult small intestine indicated that deletion of p21 has no detectable effect on the migration-associated differentiation of the four principal intestinal epithelial cell lineages or on p53-dependent apoptosis following irradiation. However, p21-/- mouse embryo fibroblasts are impaired in their ability to undergo G1 arrest following DNA damage.
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In the citing paper
“p21 is required for p53-mediated G1/S146, 147, 148 and also for G2/M cell cycle arrest.149”
From Census and evaluation of p53 target genes (2017) · cites this paper as [147]
In the citing paper
“Surprisingly, developmental senescence is not required for embryogenesis because embryos lacking p21 show minimal or no developmental defects [56].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [56]
Citations
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Cited by
Sorted by citations
CDK inhibitors: positive and negative regulators of G1-phase progression
Sherr, C. J., & Roberts, J. M. (1999) · Genes & Development · doi:10.1101/gad.13.12.1501 · Cited by 6,115
“…overexpression of catalytically inactive CDK4 can also reverse a cell cycle block imposed by p16 (Koh et al. 1995; Jiang et al. 1998) or by p53 (Latham et al. 1996), which arrests cells in G1 by inducing p21 (El-Deiry et al. 1993; Dulic et al. 1994; Brugarolas et al. 1995; Deng et al. 1995).”
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MethodSelf-citationRequirement for p53 and p21 to Sustain G 2 Arrest After DNA Damage
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“Among these, the small 165 amino acid protein p21 (also known as p21 WAF1/Cip1 ) mediates p53 -dependent G1 growth arres”
Background
Metadata
- Authors
- Brugarolas, J., Chandrasekaran, C., Gordon, J. I., Beach, D., Jacks, T., & Hannon, G. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- Washington University in St. Louis (US)
- Venue
- Nature
- Published
- 1995-10
- Volume
- 377
- Issue
- 6549
- Pages
- 552-557
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1969385456
- Cited by
- 1,242
- References
- 24
- Citations by year
- 2026: 10 · 2025: 5 · 2024: 13 · 2023: 29 · 2022: 21 · 2021: 29 · 2020: 22 · 2019: 27 · 2018: 28 · 2017: 31 · 2016: 24 · 2015: 26 · 2014: 26 · 2013: 29 · 2012: 41
- FWCI
- 33.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- p21, cell cycle arrest, radiation-induced DNA damage, G1 cell cycle arrest, cyclin-dependent kinases, PCNA, p53, apoptosis, chimeric mice, intestinal epithelial differentiation, mouse embryonic fibroblasts, cellular senescence
- MeSH terms
- Animals, Cell Cycle, Cell Differentiation, Cell Division, Cell Line, Cells, Cultured, Chimera, Enzyme Inhibitors, Gamma Rays, Intestine, Small, Mice, Inbred C57BL, Tumor Suppressor Protein p53, Cyclins, Apoptosis, Protein Serine-Threonine Kinases, Gene Targeting, Proliferating Cell Nuclear Antigen, Cyclin-Dependent Kinases, CDC2-CDC28 Kinases, Cyclin-Dependent Kinase Inhibitor p21, Cyclin-Dependent Kinase 2, Mice
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