The purpose of this project is to investigate transgenic models of human disease collaboratively with NIH scientists. Model development involves the use of both nonhomologous and homologous (targeted gene disruption, i.e. """"""""knock-out"""""""") recombination technologies. Several murine models of human disease have been the emphasis of these collaborative efforts. Our focus in these studies has been to provide a combination of gross pathologic, histopathologic, and as appropriate, ultrastructural and immunocytochemical analyses of phenotypic abnormalities and expression of these murine models. Models investigated with scientists from several ICD's include: a) Transgenic mice which express wild-type p53 b) Atm-deficient mice - a model of ataxia-telangiectasia c) p47phox deficient mice - a model of chronic granulomatous disease
