| First Author | Kühbandner S | Year | 2000 |
| Journal | Genesis | Volume | 28 |
| Issue | 1 | Pages | 15-22 |
| PubMed ID | 11020712 | Mgi Jnum | J:69325 |
| Mgi Id | MGI:1934456 | Doi | 10.1002/1526-968x(200009)28:1<15::aid-gene20>3.0.co;2-c |
| Citation | Kuhbandner S, et al. (2000) Temporally controlled somatic mutagenesis in smooth muscle. Genesis 28(1):15-22 |
| abstractText | Ligand-dependent site-specific recombinases are powerful tools to engineer the mouse genome in specific somatic cell types at selected times during pre- and postnatal development. Current efforts are primarily directed towards increasing the efficiency of this recombination system in mice. We have generated transgenic mouse lines expressing a tamoxifen-activated Cre recombinase, CreER(T2), under the control of the smooth muscle-specific SM22 promoter. Both a randomly integrated transgene [SM-CreER(T2)(tg)] and a transgene that has been 'knocked in' into the endogenous SM22 locus [SM-CreER(T2)(ki)] were expressed in smooth muscle-containing tissues. The level of CreER(T2) expression and tamoxifen-induced recombination was lower in SM-CreER(T2)(tg) mice compared with SM-CreER(T2)(ki) mice. Whereas no recombinase activity could be detected in vehicle-treated SM-CreER(T2)(ki) mice, administration of tamoxifen induced the excision of a loxP-flanked reporter transgene in up to 100% of smooth muscle cells. The recombined genome persisted for at least four months after tamoxifen treatment. SM-CreER(T2)(ki) transgenic mice should be useful to study the effects of various somatic mutations in smooth muscle. |
