The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
14-3-3σ is required to prevent mitotic catastrophe after DNA damage
Abstract
14-3-3Sigma is a member of a family of proteins that regulate cellular activity by binding and sequestering phosphorylated proteins. It has been suggested that 14-3-3sigma promotes pre-mitotic cell-cycle arrest following DNA damage, and that its expression can be controlled by the p53 tumour suppressor gene. Here we describe an improved approach to the generation of human somatic-cell knockouts, which we have used to generate human colorectal cancer cells in which both 14-3-3sigma alleles are inactivated. After DNA damage, these cells initially arrested in the G2 phase of the cell cycle, but, unlike cells containing 14-3-3sigma, the 14-3-3sigma-/- cells were unable to maintain cell-cycle arrest. The 14-3-3sigma-/- cells died ('mitotic catastrophe') as they entered mitosis. This process was associated with a failure of the 14-3-3sigma-deficient cells to sequester the proteins (cyclin B1 and cdc2) that initiate mitosis and prevent them from entering the nucleus. These results may indicate a mechanism for maintaining the G2 checkpoint and preventing mitotic death.
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“SFN (14-3-3 sigma) encodes for a protein that removes cell cycle proteins from the nucleus and is also required for the G2/M arrest.51, 157”
From Census and evaluation of p53 target genes (2017) · cites this paper as [157]
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Cites
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Cited by
Sorted by citations
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
Self-citationThe DNA damage response: putting checkpoints in perspective
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14-3-3 Proteins: Structure, Function, and Regulation
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Regulation of the G2/M transition by p53
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Metadata
- Authors
- Chan, T. A., Hermeking, H., Lengauer, C., Kinzler, K. W., & Vogelstein, B.
- Affiliations
- Johns Hopkins University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Vogelstein, Bert
- Venue
- Nature
- Published
- 1999-10-07
- Volume
- 401
- Issue
- 6753
- Pages
- 616-620
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2130603065
- Cited by
- 895
- References
- 20
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 15 · 2022: 10 · 2021: 16 · 2020: 21 · 2019: 8 · 2018: 8 · 2017: 16 · 2016: 10 · 2015: 19 · 2014: 31 · 2013: 30 · 2012: 30
- FWCI
- 21.59
- Type
- journal article
- Language
- en
- Update notices
- correction (2023-08-22)
- Open access
- closed
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Johns Hopkins University
- National Institutes of Health
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › 14-3-3 protein interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- 14-3-3 sigma, mitotic catastrophe, DNA damage, G2 checkpoint, cell cycle arrest, cyclin B1, cdc2, protein sequestration, p53, colorectal cancer cells, mitosis initiation
- MeSH terms
- Cloning, Molecular, DNA Damage, Humans, Mitosis, Proteins, Tumor Cells, Cultured, Tyrosine 3-Monooxygenase, G2 Phase, Cell Cycle Proteins, Cyclin B, cdc25 Phosphatases, 14-3-3 Proteins, Cyclin B1
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