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Targeted oncogene activation by site-specific recombination in transgenic mice.

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.

Pubmed ID: 1631115


  • Lakso M
  • Sauer B
  • Mosinger B
  • Lee EJ
  • Manning RW
  • Yu SH
  • Mulder KL
  • Westphal H


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

July 15, 1992

Associated Grants


Mesh Terms

  • Animals
  • Antigens, Polyomavirus Transforming
  • Base Sequence
  • Cataract
  • DNA Nucleotidyltransferases
  • Eye Neoplasms
  • Integrases
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • Oncogenes
  • Recombination, Genetic
  • Regulatory Sequences, Nucleic Acid
  • Viral Proteins