These transgenic mice have a tamoxifen-inducible, Cre-mediated recombination system driven by the rat elastase 1, pancreatic (Ela1) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the human estrogen receptor ligand binding domain (CreERT2). The mutant human 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. No cre activity is detectable without tamoxifen treatment. When these transgenic mice are bred with mice containing a loxP flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in Ela1
 expressing cells; making them useful in fate mapping of pancreatic acinar cells.
 Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous.

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These transgenic mice express a tamoxifen-inducible cre recombinase from the endogenous promoter/enhancer elements of the elastase 1 locus. When induced, cre activity is observed in Ela1 expressing pancreatic acinar cells; making this strain useful in fate mapping of pancreatic acinar cells.

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