Inactivation of hnRNP K by expanded intronic AUUCU repeat induces apoptosis via translocation of PKCδ to mitochondria in spinocerebellar ataxia 10

Keyphrases

• Induced Apoptosis 100%
• Mitochondria 100%
• HnRNP 100%
• Spinocerebellar Ataxia 100%
• Mitochondrium 100%
• Spinocerebellar Ataxia Type 10 70%
• Apoptosis 30%
• Transgenic Mice 20%
• Pathogenic Mechanism 20%
• Transfected Cells 20%
• Loss Function 20%
• Mouse Brain 20%
• Protein Kinase Cδ (PKCδ) 20%
• Co-immunoprecipitation (co-IP) 10%
• Overexpression 10%
• In Situ Hybridization 10%
• Activation Mechanism 10%
• Cell-to-cell 10%
• Small Interfering RNA (siRNA) 10%
• Cell Death 10%
• Genetic mutation 10%
• Disease Model 10%
• PCR Analysis 10%
• Colocalization 10%
• Caspase-3 10%
• Caspase-3 Activation 10%
• Brain Cells 10%
• Pullout 10%
• Riboprobe 10%
• Ataxin-10 10%
• Intronic RNA 10%
• K-functional 10%
• K Deficiency 10%
• ATXN10 10%
• Regulatory Targets 10%

Biochemistry, Genetics and Molecular Biology

• Mitochondrion 100%
• Programmed Cell Death 100%
• RNA 50%
• Transgenic Mouse 50%
• Caspase 3 50%
• Transcription 25%
• Immunoprecipitation 25%
• Cell Death 25%
• Intron 25%
• Gene Mutation 25%
• Reverse Transcription Polymerase Chain Reaction 25%
• RNA Probe 25%
• Ataxin 25%
• In Situ Hybridization 25%
• Deficiency 25%
• Small Interfering RNA 25%

Neuroscience

• Mitochondrion 100%
• Spinocerebellar Ataxia 100%
• Heterogeneous Nuclear Ribonucleoprotein K 100%
• Programmed Cell Death 100%
• Caspase 3 20%
• Mouse Brain 20%
• In Situ Hybridization 10%
• Immunoprecipitation 10%
• Small Interfering RNA 10%
• Cell Death 10%
• Gene Mutation 10%
• Intron 10%
• Riboprobe 10%
• Ataxin 10 10%