| Primary Identifier | MGI:2182767 | Allele Type | Transgenic |
| Attribute String | Inducible, Recombinase | Gene | Tg(CAG-cre/Esr1*)5Amc |
| Strain of Origin | (C57BL/6 x CBA)F1 | Induced With | tamoxifen |
| Is Recombinase | true | Is Wild Type | false |
| description | Homozygous transgenic mice are not viable or fertile. Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In transgenic mice the mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/Esr1 fusion protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing loxP sites flanking a sequence of interest, tamoxifen induced, Cre-mediated targeted deletions are generated in the offspring. Tamoxifen administration will induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice. Note that this transgene does not contain the cre/ERT2 fusion but was mistakenly referred to by the synonym CAG-CreERT2 in publication. J:136965 Note that this transgene does not contain the cre/ERT2 fusion but was mistakenly referred to by the synonym CAGG-CreERT2 in publication. J:130851 |
| molecularNote | This transgene expresses a fusion protein consisting of Cre recombinase joined to the ligand-binding domain of a mouse estrogen receptor modified to bind to 4-hydroxytamoxifen, but not to endogenous estrogen. The CAG promoter, containing a chicken beta actin promoter/enhancer coupled with the cytomegalovirus immediate-early (CMV-IE) enhancer, drives high levels of expression in most tissues. In the presence of tamoxifen, the fusion protein is transported into the nucleus, where cre can excise loxP-flanked segments from conditionally modified genes. |
