Genetic models of C9orf72: what is toxic?
Author:
Funder
Wellcome Trust
Publisher
Elsevier BV
Subject
Developmental Biology,Genetics
Reference87 articles.
1. Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS;DeJesus-Hernandez;Neuron,2011
2. A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD;Renton;Neuron,2011
3. Large C9orf72 hexanucleotide repeat expansions are seen in multiple neurodegenerative syndromes and are more frequent than expected in the UK population;Beck;Am J Hum Genet,2013
4. Association between repeat sizes and clinical and pathological characteristics in carriers of C9ORF72 repeat expansions (Xpansize-72): a cross-sectional cohort study;van Blitterswijk;Lancet Neurol,2013
5. How do C9ORF72 repeat expansions cause amyotrophic lateral sclerosis and frontotemporal dementia: can we learn from other noncoding repeat expansion disorders;van Blitterswijk;Curr Opin Neurol,2012
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2. PolyGR and polyPR knock-in mice reveal a conserved neuroprotective extracellular matrix signature in C9orf72 ALS/FTD neurons;Nature Neuroscience;2024-02-29
3. C9ORF72 deficiency results in degeneration of the zebrafish retinain vivo;2023-10-21
4. A monocarboxylate transporter rescues frontotemporal dementia and Alzheimer’s disease models;PLOS Genetics;2023-09-21
5. PolyGR and polyPR knock-in mice reveal a conserved neuroprotective extracellular matrix signature inC9orf72ALS/FTD neurons;2023-07-17
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