The shared genetic drivers in the KPC mouse model enabled the collection and analysis of sufficient numbers of single CTCs across different animals, yet we note significant animal-specific clustering in RNA-seq data.
In contrast, the use of the TgS100a8a9 hep mouse model enabled for the first time a detailed analysis of physiological and pathophysiological alterations in settings of low and locally restricted S100a8/a9 induction in vivo.
By treating the same xenograft multiple times, these mouse models enabled the assessment of an average response.
Specifically, mouse models enable study of how a manipulation changes the manifestation or severity of AD related disease measures such as pathology, biochemistry, cognition/behavior, synaptic/network plasticity, or survival.
Because mouse models enable targeted deletion of specific gene(s) in a defined genetic background it is possible to assess the specific function of this gene within an organism.
This project revealed how little we know about mammalian gene function, and the only way to go from there was up… Since its inception, our internationally recognized program has created hundreds of new mouse models, enabling discoveries of gene function in diverse areas such as reproduction, neurobiology, obesity, metabolism, and blood, heart and bone development.
Moreover, the BCR-ABL mouse ALL model enabled us to compare the efficacy of CY with several other commonly used anticancer drugs.
Since endothelial-specific deletion of FAK induces lethality during mouse embryonic development (Braren et al, 2006; Cohen & Guan, 2005; Ilic et al, 1995), we have generated a new mouse model that enables us to induce endothelial FAK deletion in adult mice upon tamoxifen treatment.
To trace the fate of GFRα1+ spermatogonia, we developed a knockin mouse model that enables the pulse labeling of GFRα1+ cells with persistent GFP expression, without disturbing the tissue architecture, following a single administration of 4OH-tamoxifen to GFRα1-CreER T2 ;CAG-CAT-EGFP mice.
