A DNA damage checkpoint response in telomere-initiated senescence

By F. d’Adda di Fagagna, P. Reaper, Lorena Clay-Farrace, H. Fiegler, P. Carr, T. Zglinicki, G. Saretzki, N. Carter, Stephen P. Jackson. Nature, 2003

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Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Consequently, with each cell cycle, telomeres shorten and eventually fail, generating a persistent DNA damage signal that permanently arrests growth [27].”
Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “This eventually registers as DNA damage and triggers cell cycle arrest via activation of the p53 pathway (d’Adda di Fagagna et al., 2003).”
Telomere dysfunction in ageing and age-related diseases (2022, methodology): “These include the following techniques: (1) Southern blotting, which measures mean telomere length using the length distribution of the terminal restriction fragments; (2) quantitative PCR (qPCR), which measures the ratio of telomere repeat copy number to single copy gene copy number; (3) single tel”
Cellular senescence in cancer and aging. (2007, neutral): “Based on this, dysfunctional telomeres have been visualized as foci of γH2AX that colocalize with telomeres in cultured human cells and in tissues of aged mice and baboons, providing a marker of telomere loss (d'Adda di Fagagna et al., 2003; Garcia-Cao et al., 2006; Herbig et al., 2006).”