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Neurological manifestations of knockout mice with beta-galactosidase deficiency
J Matsuda1, O Suzuki, A Oshima
1Department of Veterinary Science, National Institute of Health, Tokyo, Japan. jmatsuda@nih.go.jp
Brain & Development
|January 1, 1997
Abstract:
We succeeded in producing the beta-galactosidase-deficient knockout mouse by gene targeting in embryonic stem cells. The mutant mice developed progressive spastic diplegia within a few months after birth, and died of emaciation at 7-10 months of age. This is an authentic murine model of human GMI-gangliosidosis, and is useful for studies of its pathogenesis and treatment.