Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks

By O. Sedelnikova, I. Horikawa, D. Zimonjic, N. Popescu, W. Bonner, J. Barrett. Nature Cell Biology, 2004

811 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/9174dda425432845e30cb458ec4c7506f4aaaae1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Manuel Serrano
2. J. Campisi
3. M. Blasco
4. T. von Zglinicki
5. M. Collado
6. C. López‐Otín
7. Yihai Cao
8. A. Pendás

In Physiology

1. J. Campisi
2. Manuel Serrano
3. M. Blasco
4. M. Collado
5. T. von Zglinicki
6. C. López‐Otín
7. D. Jurk
8. Glyn Nelson

Citations in the corpus

• DNA damage response and cellular senescence in tissues of aging mice (2009, methodology): “We conclude in agreement with earlier reports (Sedelnikova et al., 2004) that stress-dependent cellular senescence in MEFs is accompanied and most probably caused by accumulation of nontelomeric DNA damage foci, so that foci formation can constitute a marker for cell senescence in murine cells.”
• Aging, Cellular Senescence, and Cancer (2012, background): “Persistent DDR signaling is generally identified by the long-term presence of nuclear DNA damage foci that contain a variety of activated DDR proteins, including activated p53 (24, 29, 42, 43).”
• The signals and pathways activating cellular senescence. (2005, neutral): “1) (Shelton, Chang, Whittier, Choi, & Funk, 1999; Serrano & Blasco, 2001; Narita et al., 2003).”
• Evolutionarily conserved and nonconserved cellular localizations and functions of human SIRT proteins. (2005, methodology): “The treatment with bleomycin (10 mU/ml for 20 h) or H2O2 (150 M for 2 h) to induce premature senescence was previously described (Sedelnikova et al., 2004).”
• Genomic instability in laminopathy-based premature aging (2005, background): “3f ), whereas in Zmpste24 −/− MEFs and in HGPS fibroblasts, a substantial number of colocalized 53BP1–γ-H2AX foci, representing irreparable DNA damag”
• Cellular senescence in cancer and aging. (2007, positive): “Organismal aging is accompanied by significant increases in DNA mutations (Vijg, 2000), DNA oxidation (Hamilton et al., 2001), chromosome losses (Rehen et al., 2005; Weaver et al., 2007), and telomereindependent γH2AX foci (Sedelnikova et al., 2004).”
• Oxidative Stress in Aging Human Skin (2015, background): “Senescence is initiated after such dramatic incidences as severe DNA damage, critical telomere shortening, oxidative stress and hyperactive oncogenic RAS [339–342].”
• Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion (2009, neutral): “, which are presumed to harbour activated oncogenes, and in aging mammalian tissue”