These transgenic mice express a tamoxifen inducible Cre recombinase driven by the rat Eno2 (enolase 2, gamma, neuronal) 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 induces Cre recombination in the granule cells of all cerebellar lobules of young (P3) and adult (P23) mice. Inducible Cre recombinase activity is also detected in a few hippocampal dentate gyrus granule cells. 
The Donating Investigator has not attempted to make this strain homozygous. Hemizygous mutant mice are viable and fertile. 







The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17&beta;-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered.

Nse-CreERT2 transgenic mice express the tamoxifen inducible cre/ERT2 fusion gene in cerebellar lobular granule cells and in a few hippocampal dentate gyrus granule cells as directed by the rat Eno2 (enolase 2, gamma, neuronal) promoter. Cre-ERT2 fusion gene activity is inducible by the administration of tamoxifen.

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