Site-specific Cre-Rat Model Generation Service Using TARGATT™ - PrimeCKO™ Conditional Knockout Rat Models - Rat Models - Animal Models - Research

TARGATT™ Site Specific Knock-In Cre-Rat Model Generation Services

 Our TARGATT™ Site-Specific Cre-Rat Model Services will advance your research with our outstanding design strategy, high-quality service, and short deliverable. Our extensive expertise in developing tissue-specific/ inducible expression rat models, reporter gene knock-in, gene overexpression, and humanized/ chimeric rat models, will help you reach your research goals quickly.  We have many options that may help you.  Below are a few proposed avenues you may be able to explore.

• Using our proprietary integrase-based TARGATT™ technology, we can insert any gene of interest (up to 20 Kb size) into a well characterized, transcriptionally active loci in the rat genome with high efficiency and with guaranteed transgene expression.

• Alternatively, you may be able to leverage our TARGATT Rat for insertion into the H11 safe harbor loci, which also results in robust transgene expression.

• In a different scenario, by taking advantage of our pre-defined human tissue-specific neurological or cardiovascular Cre-expressing promoter constructs (see list below) we can combine them with your choice of rat or simply use our established Cre-expressing Sprague Dawley rat models.

• Applied StemCell’s custom services can also help you create a custom site-specific “foxed” conditional rat model for breeding with your choice of Cre-rat model. 

• Another option is to cross bread with our existing Cre Reporter/test line that expresses GFP and LacZ.

 The temporal control of Cre activity allows the induction of genetic modifications later in embryogenesis or adult animals. This bypasses potential drawbacks such as embryonic lethality. To specifically induce temporal Cre activity, the recombinase is fused with a mutated form of the ligand-binding domain of the human estrogen receptor (ERt2). The estrogen receptor antagonist tamoxifen binds Cre-ERt2 and allows the penetration of the complex into the nucleus where Cre induces site-specific gene modification. In absence of tamoxifen, the Cre-ERt2 fusion protein remains strictly cytoplasmic.