Isolated loss of the AUTS2 long isoform, brain-wide or targeted to Calbindin-lineage cells, generates a specific suite of brain, behavioral and molecular pathologies

Neuroscience

• Exon 100%
• Hyperactivity 100%
• Brain Development 100%
• Calbindin 100%
• Behavior (Neuroscience) 50%
• In Vivo 50%
• Gene Expression 50%
• Cell Maturation 50%
• Dentate Gyrus 50%
• Promoter Region 50%
• Amnesia 50%
• Essential Gene 50%
• Granule Cell 50%
• Compulsive Behavior 50%
• Isoprotein 50%
• Calbindin 1 50%
• Hypoactivity 50%

Keyphrases

• Molecular Pathology 100%
• Behavioral Pathology 100%
• Calbindin 100%
• AUTS2 100%
• Brain Pathology 100%
• Brain Development 20%
• Ablation 13%
• Intellectual Disability 6%
• In(III) 6%
• Cell Population 6%
• Developmental Delay 6%
• Protein Isoforms 6%
• Exon 6%
• Phenotypic Effects 6%
• Hyperactivity 6%
• Downstream Genes 6%
• Loss Function 6%
• Human Patients 6%
• Alternative Promoter 6%
• Learning Memory 6%
• Developmental Behavior 6%
• Cell Lineage 6%
• Memory Deficits 6%
• Repetitive Behavior 6%
• Brain Gene Expression 6%
• Hyperactivity Disorder 6%
• Cell Maturation 6%
• Dentate Granule Cells 6%
• Behavioral Abnormalities 6%
• Genotype-phenotype Correlation 6%
• Yield Learning 6%
• Disease Presentation 6%
• Exon 8 6%
• Neuropsychiatric Disorders 6%
• Calbindin 1 6%
• Postnatal Brain 6%
• Neurodevelopmental Genes 6%
• Syndromic Disorders 6%
• Isoform Function 6%
• Regional Variants 6%
• Hypoactivity 6%
• Behavior Phenotype 6%

Biochemistry, Genetics and Molecular Biology

• Isoform 100%
• Calbindin 100%
• Brain Development 50%
• Exon 50%
• Gene Expression 25%
• Promoter Region 25%
• Protein Isoform 25%
• Cell Maturation 25%
• Cell Lineage 25%
• Essential Gene 25%
• Genotype Phenotype Correlation 25%
• Intellectual Disability 25%
• Granule Cell 25%