Lack of aspartoacylase activity disrupts survival and differentiation of neural progenitors and oligodendrocytes in a mouse model of Canavan disease

Keyphrases

• Mouse Model 100%
• White Matter 100%
• Canavan Disease 100%
• Aspartoacylase 100%
• Oligodendrocyte 100%
• Neural Progenitors 100%
• Knock-in Mouse Model 60%
• Mouse Brain 40%
• Bromodeoxyuridine 40%
• Myelin Basic Protein 40%
• Oligodendrocyte Precursor Cells 40%
• PSA-NCAM 20%
• Early Development 20%
• Pathophysiology 20%
• Cyclin-dependent Kinase 2 (CDK2) 20%
• P21Cip1 20%
• Cell Cycle Progression 20%
• Kinase Activity 20%
• Mouse Strain 20%
• Neural Stem Cells 20%
• Gene mutation 20%
• Ki-67 20%
• Dying Cells 20%
• Astrocytes 20%
• Chromatin 20%
• Large Population 20%
• Histone H3 20%
• P27Kip1 20%
• Myelinated Fibers 20%
• Severely Affected 20%
• Specific Enzymes 20%
• Protein Trafficking 20%
• Vimentin 20%
• Histone H2B 20%
• Nestin 20%
• Protein Staining 20%
• CNS Activity 20%
• SCell 20%
• PLP1 20%
• CNS Development 20%
• DM20 20%
• Mitotic Inhibitors 20%
• Massive Array 20%
• Sponginess 20%
• Noncompact 20%
• Continuous Generation 20%

Neuroscience

• Neural Stem Cell 100%
• Aspartoacylase 100%
• Oligodendrocyte 100%
• Canavan Disease 100%
• Bromodeoxyuridine 40%
• Mouse Brain 40%
• Neural Cell Adhesion Molecule 20%
• Staining Technique 20%
• Gene Mutation 20%
• Astrocyte 20%
• Kinase 20%
• Cell Cycle Progression 20%
• Histone H3 20%
• Vimentin 20%
• Myelin Basic Protein 20%
• Myelin Protein 20%
• Nestin 20%
• Proteolipid Protein 20%
• Protein Targeting 20%
• Mitotic Inhibitor 20%
• Oligodendrocyte Progenitor 20%
• Histone H2B 20%
• S Cell 20%
• Messenger RNA 20%