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This technology includes a mouse model containing a hypothetical, previously undescribed, gene that we have proven is expressed in hair cells of the inner ear and few other tissues in the body. The hair-cell limited expression of Cre is a genetic tool for creating conditional mutations affecting hair cells almost exclusively. Hair cells are the sensory receptors of both the auditory system and the vestibular system in the ears of all vertebrates.

This technology includes EPHX1/EPHX2 null mice and showed that disruption of both EPHX1 and EPHX2 almost completely abolished hydrolysis of several EETs which can be used in the treatment of cardiovascular diseases. EPHX 1 is significantly involved in EET hydrolysis, and we believe the combined use of EPHX1 and EPHX2 inhibitors would provide a better alternative to currently available therapeutic options or the EPHX2-based therapies currently in trials for the treatment of cardiovascular diseases.

This technology includes a series of recombinase responsive indicator alleles in genetically modified laboratory mice which uniquely permit non-invasive labeling of cells defined by the overlap of up to three distinct gene expression domains. In response to any combination of Cre, Flp and Dre recombinases, these alleles express high levels of eGFP and/or tdTomato that allow the visualization of cells in live and fixed tissue, including samples processed using modern tissue clearing techniques.

This technology includes a mouse model of Pompe disease, created by targeted inactivation of the acid alpha-glucosidase gene, to test novel therapies. Pompe disease is a severe muscle disorder that affects people at any age. It is a rare genetic disease caused by a deficiency of a lysosomal enzyme acid alpha-glucosidase. The enzyme degrades glycogen to glucose in the lysosomes. The deficiency leads to accumulation of glycogen in multiple organs, but cardiac and skeletal muscles are most severely affected.

This technology involves the utilization of highly effective nanobodies, specifically camelid antibodies, derived from immunized llamas to neutralize SARS-CoV-2. Additionally, it employs a unique mouse model, called a "nanomouse," that is engineered to express antibody genes from camels, alpacas, and dromedaries. These nanobodies offer significant advantages over traditional human and mouse antibodies due to their smaller size, which allows them to effectively target and bind to specific areas on antigens.

This technology includes mouse models of TL 1A diseases, such as inflammatory bowel disease and rheumatoid arthritis, to be used as a platform for studying therapeutic agents. The TNF family cytokine TL 1A co-stimulates T-cells through Its receptor and is required for autoimmune pathology driven by diverse T-cell subsets. Blocking TL 1A in mouse models of these diseases is efficacious blocking TL 1A may be useful for therapy of diseases in which TL 1A plays a pathogenic role.

This technology includes the creation of DLX3-floxed mice, specifically designed for conditional deletion of the DLX3 gene via Cre-mediated recombination. This innovative approach aims to develop mouse models for studying ectodermal dysplasia disorders. Ectodermal dysplasias are a diverse group of genetic conditions affecting the development of ectodermal structures, including hair, teeth, and bones. The DLX3f/f mice are particularly valuable for modeling specific disorders such as Tricho-dento-osseous syndrome (TDO), Amelogenesis Imperfecta (AI), and Dentinogenesis Imperfecta (DI).

This technology includes K14creDLX3 conditional knockout (cKO) mice which will be used to study ectodermal dysplasia disorders such as Amelogenesis Imperfecta, and to study molecular mechanisms of DLX3 regulation in skin and ectodermal appendages. DLX3 is expressed in the epidermis, hair matrix cells in the hair follicle and in the mesenchymal and epithelial compartment of the tooth during embryonic development. To determine the transcriptional network dependent on DLX3-function, we will generate and analyze an epithelial-specific conditional knockout of DLX3.

This technology includes mouse models that express versions of mouse cryopyrin protein containing mutations associated with human CAPS disease. We engineered mutations associated with three specific CAPS phenotypes (familial cold autoinflammatory syndrome (FCAS); Muckle-Wells syndrome (MWS); and neonatal onset multisystem inflammatory disease (NOMID)) into the mouse cryopyrin gene (called Nlrp3) to examine the roles of IL-1 β and related cytokines, and better characterize inflammasome functions.