These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Plp1, proteolipid protein (myelin) 1 promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. 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 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration allows for ablation of predetermined genes in oligodendrocytes and Schwann cells, and will also induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunohistochemical analysis of brain, optic and sciatic nerve tissue reveals that the cre/Esr1 expression mimics the endogenous promoter expression pattern. 
 <a href="https://www.jax.org/research-and-faculty/resources/cre-repository/characterized-cre-lines-jax-cre-resource">View</a> cre expression characterization.

These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Plp1, proteolipid protein (myelin) 1 promoter. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration allows for ablation of predetermined genes in oligodendrocytes and Schwann cells, and will also induce Cre recombination in developing embryos of treated mothers and in cultured cells derived from transgenic mice.

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