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Cited by 94DNA Repair MechanismsCancer-related Molecular PathwaysEffects of Radiation Exposure

DNA damage foci in mitosis are devoid of 53BP1

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Nelson, Glyn, Buhmann, Matthias, von Zglinicki, Thomas·2009·Cell Cycle
DOI 10.4161/cc.8.20.9857
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Abstract

Nuclear DNA damage foci indicate ongoing DNA damage response, which is the major inducer of cell cycle arrest, cellular senescence and apoptosis. 53BP1 is one central mediator of the DNA damage response and a component of active DNA damage foci. Using an AcGFP-53BP1c fluorescent fusion protein that quantitatively reports DNA damage, we show that the recruitment of 53BP1 into gammaH2A.X-containing DNA damage foci was inhibited at G(2)/M. This suggests a possible mechanism for cells to continue through the G(2) checkpoint with gammaH2A.X-flagged double strand breaks via inhibition of 53BP1-mediated DNA damage signalling.

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  • The AcGFP-53BP1c fusion protein quantitatively reports foci dynamics in live cells.

    “We fused a large C-terminal fragment of 53BP1, containing both the TUDOR and BRCT domains necessary for focus formation and interaction with TP53, to GFP, producing an AcGFP–53BP1c fusion protein that quantitatively reported foci dynamics in live cells (Nelson et al, 2009).”

    From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Nelson et al, 2009

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Authors
Nelson, G., Buhmann, M., & von Zglinicki, T.
Affiliations
Newcastle University (GB)
ORCID
Venue
Cell Cycle
Publisher
Informa UK Limited
Published
2009-10-15
Volume
8
Issue
20
Pages
3379-3383
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
DOI
10.4161/cc.8.20.9857
OpenAlex
W2063767314
Cited by
94
References
0
Citations by year
2026: 3 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 4 · 2021: 5 · 2020: 5 · 2019: 4 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 13 · 2013: 5 · 2012: 12
FWCI
3.49
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed (publishedVersion)
  • Newcastle University ePrints (Newcastle Univesity)
Funders
Biotechnology and Biological Sciences Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Keywords
53BP1, DNA damage foci, mitosis, G2/M checkpoint, γH2AX, DNA double-strand breaks, DNA damage response, cell cycle checkpoints
MeSH terms
Tumor Suppressor p53-Binding Protein 1, Cell Division, Cell Line, DNA Damage, Histones, Humans, Mitosis, Phosphorylation, Recombinant Fusion Proteins, Signal Transduction, G2 Phase, Intracellular Signaling Peptides and Proteins

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