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.
Dates
Type | When |
---|---|
Created | 19 years, 2 months ago (May 31, 2006, 8:05 a.m.) |
Deposited | 3 years, 4 months ago (April 13, 2022, 1:02 p.m.) |
Indexed | 7 hours, 57 minutes ago (Aug. 29, 2025, 6:08 a.m.) |
Issued | 33 years, 1 month ago (July 15, 1992) |
Published | 33 years, 1 month ago (July 15, 1992) |
Published Online | 33 years, 1 month ago (July 15, 1992) |
Published Print | 33 years, 1 month ago (July 15, 1992) |
@article{Lakso_1992, title={Targeted oncogene activation by site-specific recombination in transgenic mice.}, volume={89}, ISSN={1091-6490}, url={http://dx.doi.org/10.1073/pnas.89.14.6232}, DOI={10.1073/pnas.89.14.6232}, number={14}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Lakso, M and Sauer, B and Mosinger, B and Lee, E J and Manning, R W and Yu, S H and Mulder, K L and Westphal, H}, year={1992}, month=jul, pages={6232–6236} }