A mouse model of classical late-infantile neuronal ceroid lipofuscinosis based on targeted disruption of the CLN2 gene results in a loss of tripeptidyl-peptidase I activity and progressive neurodegeneration

David E. Sleat, Jennifer A. Wiseman, Mukarram El-Banna, Kwi Hye Kim, Qinwen Mao, Sandy Price, Shannon L. Macauley, Richard L. Sidman, Michael M. Shen, Qi Zhao, Marco A. Passini, Beverly L. Davidson, Gregory R. Stewart, Peter Lobel*

*Corresponding author for this work

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Medicine and Dentistry

Neuroscience

Biochemistry, Genetics and Molecular Biology