Galnt17 loss-of-function leads to developmental delay and abnormal coordination, activity, and social interactions with cerebellar vermis pathology

Keyphrases

• Developmental Delay 100%
• Social Interaction 100%
• Loss Function 100%
• Coordinated Operation 100%
• Coordination Interaction 100%
• Cerebellar Vermis 100%
• AUTS2 100%
• Williams-Beuren Syndrome 100%
• Abnormal Coordination 100%
• Cell Adhesion 50%
• Neurotransmitters 50%
• Neurite 50%
• Brain Development 50%
• Cerebellum 50%
• O-linked Glycosylation 50%
• Knock-in Mouse Model 50%
• Cell Signaling 50%
• Adhesion Cell 50%
• Transcriptome Analysis 50%
• Protein Analysis 50%
• Neuropathology 50%
• Neurite Outgrowth 50%
• Neurodevelopment 50%
• Behavioral Phenotype 50%
• Genomic Regions 50%
• Knockout mutant 50%
• Molecular Data 50%
• In Vivo Function 50%
• Activity Coordination 50%
• Synaptic Signaling 50%
• Abnormal Activity 50%
• N-acetylglucosaminyltransferase 50%
• Heparan Sulfate 50%
• Neuronal Differentiation 50%
• Neurodevelopmental Phenotypes 50%
• Mucin-type O-glycan 50%
• Molecular Phenotype 50%
• Axon Pathfinding 50%
• Brain Phenotypes 50%
• Mucin-type 50%
• Developmental Neuropathology 50%
• Social Interaction Deficits 50%
• Brain Pathology 50%

Neuroscience

• Social Interaction 100%
• Glycosylation 100%
• Williams Syndrome 100%
• Cerebellar Vermis 100%
• Mucin 100%
• Cell Adhesion 50%
• Neurotransmitter 50%
• In Vivo 50%
• Neurite 50%
• Cell Signaling 50%
• Cerebellum 50%
• Neurite Outgrowth 50%
• Nerve Cell Differentiation 50%
• Transcriptomics 50%
• Brain Development 50%
• Axon Guidance 50%
• N Acetylgalactosaminyltransferase 50%
• Heparan Sulfate 50%