J. Wiseman

发表

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

R. Sidman, Q. Mao, B. Davidson, 2004, The Journal of Neuroscience.

Analysis of Brain and Cerebrospinal Fluid from Mouse Models of the Three Major Forms of Neuronal Ceroid Lipofuscinosis Reveals Changes in the Lysosomal Proteome*

Caifeng Zhao, D. Sleat, Haiyan Zheng, 2019, Molecular & Cellular Proteomics.

Inducible transgenic expression of tripeptidyl peptidase 1 in a mouse model of late-infantile neuronal ceroid lipofuscinosis

D. Sleat, P. Lobel, Mukarram El-Banna, 2018, PloS one.

Proteomic Analysis of Brain and Cerebrospinal Fluid from the Three Major Forms of Neuronal Ceroid Lipofuscinosis Reveals Potential Biomarkers.

Caifeng Zhao, K. Sims, D. Sleat, 2017, Journal of proteome research.

A Basic ApoE-Based Peptide Mediator to Deliver Proteins across the Blood-Brain Barrier: Long-Term Efficacy, Toxicity, and Mechanism.

W. Banks, K. Reuhl, R. Daneman, 2017, Molecular therapy : the journal of the American Society of Gene Therapy.

Chronic Enzyme Replacement to the Brain of a Late Infantile Neuronal Ceroid Lipofuscinosis Mouse Has Differential Effects on Phenotypes of Disease

J. Millonig, D. Sleat, D. Moore, 2017, Molecular therapy. Methods & clinical development.

Extending the Mannose 6-Phosphate Glycoproteome by High Resolution/Accuracy Mass Spectrometry Analysis of Control and Acid Phosphatase 5-Deficient Mice*

D. Sleat, Haiyan Zheng, D. Moore, 2013, Molecular & Cellular Proteomics.

Allele frequency and likely impact of the glycogen branching enzyme deficiency gene in Quarter Horse and Paint Horse populations.

J. Mickelson, M. Penedo, S. Valberg, 2006, Journal of veterinary internal medicine.

Genetic evidence for nonredundant functional cooperativity between NPC1 and NPC2 in lipid transport.

M. Shen, S. Walkley, D. Sleat, 2004, Proceedings of the National Academy of Sciences of the United States of America.

Proteomic analysis of mouse models of Niemann‐Pick C disease reveals alterations in the steady‐state levels of lysosomal proteins within the brain

D. Sleat, Haiyan Zheng, D. Moore, 2012, Proteomics.

A mouse mutant deficient in both neuronal ceroid lipofuscinosis‐associated proteins CLN3 and TPP1

J. Cooper, D. Sleat, P. Lobel, 2023, Journal of inherited metabolic disease.