Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a).

By U. Herbig, Wendy A. Jobling, B. Chen, David J. Chen, John M. Sedivy. Molecules and Cells, 2004

1,357 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/f6f7d5539447448bc59bab52f899b2cb12b03c99

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Citations in the corpus

Shelterin: the protein complex that shapes and safeguards human telomeres. (2005, positive): “ATR has been implicated as the second transducer by experiments on cells with shortened telomeres (Herbig et al. 2004).”
Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all (2006, background): “However, opinions are divided on whether and how INK4a is activated by telomere loss or other forms of DNA damag”
Cellular senescence and its effector programs (2014, background): “…shown that the DDR kinases are activated during replicative senescence, which is associated with the gradual shortening of telomeres (Harley et al. 1990), and pairwise inhibition of ATM/ATR or CHK2/CHK1 delays the onset of replicative senescence (d’Adda di Fagagna et al. 2003; Herbig et al. 2004).”
Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “Damage sensor proteins, such as ATM in the replicative senescence of human cells, recognize a stress—for example short telomeres— and activate a master regulator (generally p53 through ATMdependent phosphorylation), which in turn upregulates effectors of cell cycle arrest [8].”
Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Senescent cells are detected in culture and in vivo by a variety of markers, including the senescence-associated β-galactosidase (SAβgal) [28], p16 [39], telomere-associated DNA damage foci [40], senescence-associated heterochromatin foci [41], and several other molecules; all of these markers have ”
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”
DNA damage response and cellular senescence in tissues of aging mice (2009, background): “DNA double strand breaks as well as telomere uncapping (d’Adda di Fagagna et al., 2003; Herbig et al., 2004; Takai et al., 2004) induce a DNA damage response.”
An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “Telomere shortening, acting through a pathway involving p53, is one of the most well-documented triggers for cellular senescence (101).”