Genome instability independent of type I interferon signaling drives neuropathology caused by impaired ribonucleotide excision repair

Keyphrases

• Neuropathology 100%
• Genomic Instability 100%
• Nucleotide Excision Repair 100%
• Type I Interferon Signaling 100%
• Neuroinflammation 75%
• Ribonuclease H2 75%
• Cyclic GMP-AMP Synthase (cGAS) 50%
• Aicardi 50%
• DNA Damage 25%
• Neurodegeneration 25%
• Neurogenesis 25%
• Ribonucleotides 25%
• Factor-critical 25%
• Interferon-α (IFN-α) 25%
• Ataxia 25%
• Responsive Genes 25%
• DNA Damage Signaling 25%
• DNA Integrity 25%
• Monogenic 25%
• Neurodevelopmental 25%
• Non-homologous End Joining 25%
• Dependent Types 25%
• Nucleic Acid Metabolism 25%
• Anti-neuroinflammation 25%
• Cerebellar Development 25%
• Genomic Surveillance 25%
• Neurodevelopmental Defects 25%
• RNase H2 25%
• Type I Interferonopathy 25%
• RNASEH2B 25%

Biochemistry, Genetics and Molecular Biology

• Genome Instability 100%
• Base Excision Repair 100%
• Nucleotide Excision Repair 100%
• Drive 100%
• Interferon Type I 100%
• Ribonucleotide 100%
• Ribonuclease 75%
• DNA Damage 50%
• Upregulation 25%
• Nervous System Development 25%
• P53 25%
• Non-Homologous End Joining 25%
• Nucleic Acid Metabolism 25%
• Interferon 25%