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Times Cited: 173
Times Cited: 173
Times Cited
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Similarity
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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C9orf72 BAC Transgenic Mice Display Typical Pathologic Features of ALS/FTD.
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C9orf72 BAC Mouse Model with Motor Deficits and Neurodegenerative Features of ALS/FTD.
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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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C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins.
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Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS.
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Neurodegeneration. C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits.
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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.
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RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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C9orf72 is required for proper macrophage and microglial function in mice.
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RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.
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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.
Clotilde Lagier-Tourenne, Michael Baughn, Frank Rigo, Shuying Sun, Patrick Liu, Hai-Ri Li, Jie Jiang, Andrew T Watt, Seung Chun, Melanie Katz,[...]. Proc Natl Acad Sci U S A 2013
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C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits.
Max Koppers, Anna M Blokhuis, Henk-Jan Westeneng, Margo L Terpstra, Caroline A C Zundel, Renata Vieira de Sá, Raymond D Schellevis, Adrian J Waite, Derek J Blake, Jan H Veldink,[...]. Ann Neurol 2015
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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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Loss-of-function mutations in the C9ORF72 mouse ortholog cause fatal autoimmune disease.
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Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells.
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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.
Tania F Gendron, Kevin F Bieniek, Yong-Jie Zhang, Karen Jansen-West, Peter E A Ash, Thomas Caulfield, Lillian Daughrity, Judith H Dunmore, Monica Castanedes-Casey, Jeannie Chew,[...]. Acta Neuropathol 2013
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Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion.
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Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
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Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS.
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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 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.
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C9orf72 nucleotide repeat structures initiate molecular cascades of disease.
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C9orf72 Dipeptide Repeats Impair the Assembly, Dynamics, and Function of Membrane-Less Organelles.
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Hexanucleotide repeats in ALS/FTD form length-dependent RNA foci, sequester RNA binding proteins, and are neurotoxic.
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Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins.
Kohji Mori, Thomas Arzberger, Friedrich A Grässer, Ilse Gijselinck, Stephanie May, Kristin Rentzsch, Shih-Ming Weng, Martin H Schludi, Julie van der Zee, Marc Cruts,[...]. Acta Neuropathol 2013
Kohji Mori, Thomas Arzberger, Friedrich A Grässer, Ilse Gijselinck, Stephanie May, Kristin Rentzsch, Shih-Ming Weng, Martin H Schludi, Julie van der Zee, Marc Cruts,[...]. Acta Neuropathol 2013
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C9orf72 ablation causes immune dysregulation characterized by leukocyte expansion, autoantibody production, and glomerulonephropathy in mice.
Amanda Atanasio, Vilma Decman, Derek White, Meg Ramos, Burcin Ikiz, Hoi-Ching Lee, Chia-Jen Siao, Susannah Brydges, Elizabeth LaRosa, Yu Bai,[...]. Sci Rep 2016
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Decoding ALS: from genes to mechanism.
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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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Poly(GR) impairs protein translation and stress granule dynamics in C9orf72-associated frontotemporal dementia and amyotrophic lateral sclerosis.
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C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration.
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C9orf72 frontotemporal lobar degeneration is characterised by frequent neuronal sense and antisense RNA foci.
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A C9orf72 promoter repeat expansion in a Flanders-Belgian cohort with disorders of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum: a gene identification study.
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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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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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Differential Toxicity of Nuclear RNA Foci versus Dipeptide Repeat Proteins in a Drosophila Model of C9ORF72 FTD/ALS.
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Spinal poly-GA inclusions in a C9orf72 mouse model trigger motor deficits and inflammation without neuron loss.
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Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers.
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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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Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress.
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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.