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Times Cited: 174
Times Cited
Times Co-cited
Similarity
Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation.
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Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence.
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Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication.
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Factors that influence telomeric oxidative base damage and repair by DNA glycosylase OGG1.
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DNA damage foci at dysfunctional telomeres.
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Super-resolution fluorescence imaging of telomeres reveals TRF2-dependent T-loop formation.
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Removal of shelterin reveals the telomere end-protection problem.
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Protection of telomeres through independent control of ATM and ATR by TRF2 and POT1.
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Oxidative stress induces persistent telomeric DNA damage responsible for nuclear morphology change in mammalian cells.
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Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts.
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Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence.
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Mitochondrial localization of telomeric protein TIN2 links telomere regulation to metabolic control.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.