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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
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Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS.
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RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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C9orf72 nucleotide repeat structures initiate molecular cascades of disease.
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C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins.
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Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS.
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Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells.
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Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death.
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C9orf72 Dipeptide Repeats Impair the Assembly, Dynamics, and Function of Membrane-Less Organelles.
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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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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study.
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Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
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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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RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention.
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Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins.
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C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.
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Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS.
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Non-ATG-initiated translation directed by microsatellite expansions.
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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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Neurodegeneration. C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits.
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C9orf72 is required for proper macrophage and microglial function in mice.
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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.
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Reduced C9orf72 protein levels in frontal cortex of amyotrophic lateral sclerosis and frontotemporal degeneration brain with the C9ORF72 hexanucleotide repeat expansion.
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Poly(GR) in C9ORF72-Related ALS/FTD Compromises Mitochondrial Function and Increases Oxidative Stress and DNA Damage in iPSC-Derived Motor Neurons.
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Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6.
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A C9ORF72/SMCR8-containing complex regulates ULK1 and plays a dual role in autophagy.
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Sense-encoded poly-GR dipeptide repeat proteins correlate to neurodegeneration and uniquely co-localize with TDP-43 in dendrites of repeat-expanded C9orf72 amyotrophic lateral sclerosis.
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C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking.
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The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy.
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TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis.
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Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
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Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72.
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Nucleolar stress and impaired stress granule formation contribute to C9orf72 RAN translation-induced cytotoxicity.
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C9orf72 BAC Mouse Model with Motor Deficits and Neurodegenerative Features of ALS/FTD.
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C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration.
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Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers.
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Differential Toxicity of Nuclear RNA Foci versus Dipeptide Repeat Proteins in a Drosophila Model of C9ORF72 FTD/ALS.
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Drosophila screen connects nuclear transport genes to DPR pathology in c9ALS/FTD.
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C9orf72 frontotemporal lobar degeneration is characterised by frequent neuronal sense and antisense RNA foci.
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Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing.
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C9orf72 hexanucleotide repeat associated with amyotrophic lateral sclerosis and frontotemporal dementia forms RNA G-quadruplexes.
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Expanded GGGGCC repeat RNA associated with amyotrophic lateral sclerosis and frontotemporal dementia causes neurodegeneration.
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The disease-associated r(GGGGCC)n repeat from the C9orf72 gene forms tract length-dependent uni- and multimolecular RNA G-quadruplex structures.
Kaalak Reddy, Bita Zamiri, Sabrina Y R Stanley, Robert B Macgregor, Christopher E Pearson. J Biol Chem 2013
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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.