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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Clin Immunol. 2015 Mar 28;158(2):193–203. doi: 10.1016/j.clim.2015.03.017

Fig. 1.

Fig. 1

Schematic representation of the Tet-On transgenic mouse model. This double transgenic mouse (dnPKCδ+/CD2-rtTA+) results from the breeding of two different strains of mice. One strain expresses the reverse tetracycline-controlled transactivator (rtTA) which comprises the TetR repressor and the VP16 transactivation domain. This vector is driven by the CD2 promoter (CD2+ cell-specific, PCD2), which causes rtTA expression only in CD2+ cells. The other strain expresses the dnPKCδ (PKCδ cDNA) under the control of a tetracycline-responding element (TRE). As consequence, the double transgenic mouse responds with transcription of the transgene only in the presence of the tetracycline derivative, doxycycline (doxy). In the absence of doxycycline, the transcription cannot be completed.