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Times Cited: 175
Times Cited: 175
Times Cited
Times Co-cited
Similarity
Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation.
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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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Targeted and Persistent 8-Oxoguanine Base Damage at Telomeres Promotes Telomere Loss and Crisis.
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Defective repair of oxidative base lesions by the DNA glycosylase Nth1 associates with multiple telomere defects.
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Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.
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Human telomeres are hypersensitive to UV-induced DNA Damage and refractory to repair.
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Mitochondrial localization of telomeric protein TIN2 links telomere regulation to metabolic control.
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Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan.
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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.