Targeted oncogene activation by site-specific recombination in transgenic mice

  1. M Lakso,
  2. B Sauer,
  3. B Mosinger, Jr,
  4. E J Lee,
  5. R W Manning,
  6. S H Yu,
  7. K L Mulder, and
  8. H Westphal
  1. Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.

Abstract

An efficient and accurate method for controlled in vivo transgene modulation by site-directed recombination is described. Seven transgenic mouse founder lines were produced carrying the murine lens-specific alpha A-crystallin promoter and the simian virus 40 large tumor-antigen gene sequence, separated by a 1.3-kilobase-pair Stop sequence that contains elements preventing expression of the large tumor-antigen gene and Cre recombinase recognition sites. Progeny from two of these lines were mated with transgenic mice expressing the Cre recombinase under control of either the murine alpha A-crystallin promoter or the human cytomegalovirus promoter. All double-transgenic offspring developed lens tumors. Subsequent analysis confirmed that tumor formation resulted from large tumor-antigen activation via site-specific, Cre-mediated deletion of Stop sequences.

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  1. PNAS July 15, 1992 vol. 89 no. 14 6232-6236
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