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Molecular Therapy. Methods & Clinical Development|October 6, 2025
Elevated tripeptidyl-peptidase 1 corrects multiple disease phenotypes in a mouse model of juvenile neuronal ceroid lipofuscinosisWhitney Banach-Petrosky, Katherine E Larrimore, Elizabeth H Sleat, et al.
Human Mutation|July 14, 2017
Using whole-exome sequencing to investigate the genetic bases of lysosomal storage diseases of unknown etiologyNan Wang, Yeting Zhang, Erika Gedvilaite, et al.
Molecular Genetics and Metabolism|July 26, 2011
Intrathecal tripeptidyl-peptidase 1 reduces lysosomal storage in a canine model of late infantile neuronal ceroid lipofuscinosisBrian R Vuillemenot, Martin L Katz, Joan R Coates, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|October 16, 2004
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 neurodegenerationDavid E Sleat, Jennifer A Wiseman, Mukarram El-Banna, et al.
Molecular Therapy : the Journal of the American Society of Gene Therapy|July 20, 2007
Timing of therapeutic intervention determines functional and survival outcomes in a mouse model of late infantile batten diseaseMario A Cabrera-Salazar, Eric M Roskelley, Jie Bu, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|February 3, 2006
Intracranial delivery of CLN2 reduces brain pathology in a mouse model of classical late infantile neuronal ceroid lipofuscinosisMarco A Passini, James C Dodge, Jie Bu, et al.
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