Wan Yun Ho, Sheeja Navakkode, Fujia Liu, Tuck Wah Soong, Shuo-Chien Ling. Acta Neuropathol Commun 2020
Times Cited: 11
Times Cited: 11
Times Cited
Times Co-cited
Similarity
Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
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Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion.
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Novel antibodies reveal presynaptic localization of C9orf72 protein and reduced protein levels in C9orf72 mutation carriers.
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C9orf72-mediated ALS and FTD: multiple pathways to disease.
Rubika Balendra, Adrian M Isaacs. Nat Rev Neurol 2018
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C9ORF72 repeat expansion causes vulnerability of motor neurons to Ca2+-permeable AMPA receptor-mediated excitotoxicity.
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Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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Synaptic dysfunction induced by glycine-alanine dipeptides in C9orf72-ALS/FTD is rescued by SV2 replenishment.
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Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability.
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Distinct brain transcriptome profiles in C9orf72-associated and sporadic ALS.
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C9ORF72-ALS/FTD-associated poly(GR) binds Atp5a1 and compromises mitochondrial function in vivo.
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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.
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Altered calcium dynamics and glutamate receptor properties in iPSC-derived motor neurons from ALS patients with C9orf72, FUS, SOD1 or TDP43 mutations.
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RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.
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The expanding biology of the C9orf72 nucleotide repeat expansion in neurodegenerative disease.
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Synaptic localization of C9orf72 regulates post-synaptic glutamate receptor 1 levels.
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Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for amyotrophic lateral sclerosis.
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Dendritic spinopathy in transgenic mice expressing ALS/dementia-linked mutant UBQLN2.
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Pathophysiological and diagnostic implications of cortical dysfunction in ALS.
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Cortical synaptic and dendritic spine abnormalities in a presymptomatic TDP-43 model of amyotrophic lateral sclerosis.
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Repeat-associated non-AUG translation in C9orf72-ALS/FTD is driven by neuronal excitation and stress.
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Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs.
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Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death.
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The ALS/FTLD associated protein C9orf72 associates with SMCR8 and WDR41 to regulate the autophagy-lysosome pathway.
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RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention.
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Human C9ORF72 Hexanucleotide Expansion Reproduces RNA Foci and Dipeptide Repeat Proteins but Not Neurodegeneration in BAC Transgenic Mice.
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C9orf72 nucleotide repeat structures initiate molecular cascades of disease.
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C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration.
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C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.
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C9orf72 and RAB7L1 regulate vesicle trafficking in amyotrophic lateral sclerosis and frontotemporal dementia.
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C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins.
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C9ORF72 expression and cellular localization over mouse development.
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Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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Impairment of Mitochondrial Calcium Buffering Links Mutations in C9ORF72 and TARDBP in iPS-Derived Motor Neurons from Patients with ALS/FTD.
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Synaptic Paths to Neurodegeneration: The Emerging Role of TDP-43 and FUS in Synaptic Functions.
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C9ORF72 interaction with cofilin modulates actin dynamics in motor neurons.
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Reduced C9orf72 function leads to defective synaptic vesicle release and neuromuscular dysfunction in zebrafish.
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Cortical hyperexcitability may precede the onset of familial amyotrophic lateral sclerosis.
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Neonatal neuronal circuitry shows hyperexcitable disturbance in a mouse model of the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.
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Cortical hyperexcitability in patients with C9ORF72 mutations: Relationship to phenotype.
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Synapse Dysfunction of Layer V Pyramidal Neurons Precedes Neurodegeneration in a Mouse Model of TDP-43 Proteinopathies.
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Mutant C9orf72 human iPSC-derived astrocytes cause non-cell autonomous motor neuron pathophysiology.
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Cortical hyperexcitability precedes lower motor neuron dysfunction in ALS.
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Changes in the Excitability of Neocortical Neurons in a Mouse Model of Amyotrophic Lateral Sclerosis Are Not Specific to Corticospinal Neurons and Are Modulated by Advancing Disease.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.