DNA repair is crucial for maintaining hematopoietic stem cell function

Research output: Contribution to journalArticle

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Abstract

Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80-/- mice defective in NHEJ and telomere maintenance, XpdTTD mice defective in nucleotide excision repair, and late generation mTr-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.

Original languageEnglish (US)
Pages (from-to)523-529
Number of pages7
JournalDNA Repair
Volume7
Issue number3
DOIs
StatePublished - Mar 1 2008
Externally publishedYes

Keywords

  • Aging
  • Endogenous damage
  • Oxidative stress
  • Progeria

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