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August 15, 1992Proceedings of the National Academy of SciencesOpen Access

A pattern of accumulation of a somatic deletion of mitochondrial DNA in aging human tissues.

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GCGino CortopassiUniversity of California, DavisDSDarryl ShibataUniversity of GenevaNSNay-Wei SoongMaxygen (United States)

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Cortopassi et al. (1992) studied this question.

synapsesocial.com/papers/69df2b57de200760a8614867https://doi.org/10.1073/pnas.89.16.7370
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Chloroplast and Mitochondrial Mechanisms for Protection Against Oxygen Toxicity1991 · 72 citations
  2. 2DNA damage promotes jumping between templates during enzymatic amplification.1990 · 506 citations
  3. 3The Absence of a Pyrimidine Dimer Repair Mechanism in Mammalian Mitochondria1974 · 536 citations
  4. 4Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction.1991 · 556 citations