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Article

DNA end joining becomes less efficient and more error-prone during cellular senescence.

Proceedings of the National Academy of Sciences of the United States of America - 18 May 2004

Seluanov Andrei, Mittelman David, Pereira-Smith Olivia M, Wilson John H, Gorbunova Vera

Abstract excerpt

Accumulation of somatic mutations is thought to contribute to the aging process. Genomic instability has been shown to increase during aging, suggesting an aberrant function of DNA double-strand break (DSB) repair. Surprisingly, DSB repair has not been examined with respect to cellular senescence. Therefore, we have studied the ability of young, presenescent, and senescent normal human fibroblasts to repair DSBs...

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Identifiers

PMID: 15123826
DOI: 10.1073/pnas.0400726101
PMCID: PMC419656

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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