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Cellular Werner phenotypes in mice expressing a putative dominant-negative human WRN gene.

Mutations at the Werner helicase locus (WRN) are responsible for the Werner syndrome (WS). WS patients prematurely develop an aged appearance and various age-related disorders. We have generated transgenic mice expressing human WRN with a putative dominant-negative mutation (K577M-WRN). Primary tail fibroblast cultures from K577M-WRN mice showed three characteristics of WS cells: hypersensitivity to 4-nitroquinoline-1-oxide (4NQO), reduced replicative potential, and reduced expression of the endogenous WRN protein. These data suggest that K577M-WRN mice may provide a novel mouse model for the WS.

Pubmed ID: 10628995


  • Wang L
  • Ogburn CE
  • Ware CB
  • Ladiges WC
  • Youssoufian H
  • Martin GM
  • Oshima J



Publication Data

January 17, 2000

Associated Grants

  • Agency: NIA NIH HHS, Id: P01 AG01751
  • Agency: NIA NIH HHS, Id: R01 AG14446
  • Agency: NCI NIH HHS, Id: R24 CA78088

Mesh Terms

  • 4-Nitroquinoline-1-oxide
  • Alleles
  • Animals
  • Cell Division
  • DNA Helicases
  • Down-Regulation
  • Exodeoxyribonucleases
  • Genes, Dominant
  • Humans
  • Mice
  • Mice, Transgenic
  • Phenotype
  • Quinolones
  • RecQ Helicases
  • Werner Syndrome