The Center for Transgene Research at the University of Notre Dame was established in 1995 to develop and employ mice with designed gene alterations to study functions of components of the hemostasis system in a variety of genetic diseases. It was renamed the W. M. Keck Center for Transgene Research in 1998, after receipt of funding from the W. M. Keck Foundation to significantly expand its infrastructure.
The mission of the center is to develop and use gene-targeting technology to investigate the pathophysiological roles of the genes of the blood coagulation, anticoagulation, and fibrinolytic pathways in hemostasis, with associated relevance to embryonic development, cancer, infection, and inflammation. Toward this end, the foci of the center have been directed in several complementary programs. One major effort of the center is to use novel gene-targeting and transgenic strategies, as well as sophisticated genetic manipulations, to generate mice with partial and complete deficiencies, as well as modifications of several hemostasis genes.
The Notre Dame W. M. Keck Center is maintaining perhaps the largest collection of mice with modified hemostatic systems in the world. A major effort of this Center is to employ these hemostasis-altered animal models to study several acute and chronic inflammatory diseases (particularly, sepsis, cardiac fibrosis, asthma, cancer, and neurodegenerative maladies) in order to understand mechanistically the basis of the critically important crosstalk between hemostasis and inflammation.
Our neurological program has led to the development of pharmacological and electrophysiological tools to study neuronal circuitry and intrinsic electrical functions of neurons, and how they are impacted during an ischemic stroke which we believe will lead towards the development of effective therapeutic approaches.
Our translational program extents to collaborations with Memorial Hospital trauma surgeons and emergency room physicians in developing models of traumatic brain injury to further characterize the associated coagulopathies of these injuries.
In the end, it is our hope to understand the molecular basis of diseases which rank among the leading causes of mortality and morbidity of humans, with the expectation that novel diagnostic and subsequent interventional strategies can be designed for humans.