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Times Cited: 49
Times Cited: 49
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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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
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RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.
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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS.
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C9ORF72 GGGGCC repeat-associated non-AUG translation is upregulated by stress through eIF2α phosphorylation.
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RAN translation at C9orf72-associated repeat expansions is selectively enhanced by the integrated stress response.
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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS.
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Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
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C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins.
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CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts.
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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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Non-ATG-initiated translation directed by microsatellite expansions.
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RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention.
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CRISPR-Cas9 Screens Identify the RNA Helicase DDX3X as a Repressor of C9ORF72 (GGGGCC)n Repeat-Associated Non-AUG Translation.
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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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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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Phase Separation of C9orf72 Dipeptide Repeats Perturbs Stress Granule Dynamics.
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Translation of dipeptide repeat proteins from the C9ORF72 expanded repeat is associated with cellular stress.
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C9orf72 Dipeptide Repeats Impair the Assembly, Dynamics, and Function of Membrane-Less Organelles.
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Repeat-associated non-AUG translation in C9orf72-ALS/FTD is driven by neuronal excitation and stress.
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Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells.
Ilmin Kwon, Siheng Xiang, Masato Kato, Leeju Wu, Pano Theodoropoulos, Tao Wang, Jiwoong Kim, Jonghyun Yun, Yang Xie, Steven L McKnight. Science 2014
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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.
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C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration.
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C9orf72 nucleotide repeat structures initiate molecular cascades of disease.
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C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.
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Heterochromatin anomalies and double-stranded RNA accumulation underlie C9orf72 poly(PR) toxicity.
Yong-Jie Zhang, Lin Guo, Patrick K Gonzales, Tania F Gendron, Yanwei Wu, Karen Jansen-West, Aliesha D O'Raw, Sarah R Pickles, Mercedes Prudencio, Yari Carlomagno,[...]. Science 2019
Yong-Jie Zhang, Lin Guo, Patrick K Gonzales, Tania F Gendron, Yanwei Wu, Karen Jansen-West, Aliesha D O'Raw, Sarah R Pickles, Mercedes Prudencio, Yari Carlomagno,[...]. Science 2019
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Hexanucleotide repeats in ALS/FTD form length-dependent RNA foci, sequester RNA binding proteins, and are neurotoxic.
Youn-Bok Lee, Han-Jou Chen, João N Peres, Jorge Gomez-Deza, Jan Attig, Maja Stalekar, Claire Troakes, Agnes L Nishimura, Emma L Scotter, Caroline Vance,[...]. Cell Rep 2013
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Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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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
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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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Nucleolar stress and impaired stress granule formation contribute to C9orf72 RAN translation-induced cytotoxicity.
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Drosophila screen connects nuclear transport genes to DPR pathology in c9ALS/FTD.
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eIF4B and eIF4H mediate GR production from expanded G4C2 in a Drosophila model for C9orf72-associated ALS.
Lindsey D Goodman, Mercedes Prudencio, Ananth R Srinivasan, Olivia M Rifai, Virginia M-Y Lee, Leonard Petrucelli, Nancy M Bonini. Acta Neuropathol Commun 2019
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Toxic PRn poly-dipeptides encoded by the C9orf72 repeat expansion block nuclear import and export.
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CRISPR-Cas9 screens in human cells and primary neurons identify modifiers of C9ORF72 dipeptide-repeat-protein toxicity.
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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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Neurodegeneration. C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits.
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The Role of Dipeptide Repeats in C9ORF72-Related ALS-FTD.
Brian D Freibaum, J Paul Taylor. Front Mol Neurosci 2017
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Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions.
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Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers.
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C9ORF72-ALS/FTD-associated poly(GR) binds Atp5a1 and compromises mitochondrial function in vivo.
So Yoen Choi, Rodrigo Lopez-Gonzalez, Gopinath Krishnan, Hannah L Phillips, Alissa Nana Li, William W Seeley, Wei-Dong Yao, Sandra Almeida, Fen-Biao Gao. Nat Neurosci 2019
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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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Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress.
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A Liquid-to-Solid Phase Transition of the ALS Protein FUS Accelerated by Disease Mutation.
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RAN Translation in Huntington Disease.
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CGG Repeat-Associated Non-AUG Translation Utilizes a Cap-Dependent Scanning Mechanism of Initiation to Produce Toxic Proteins.
Michael G Kearse, Katelyn M Green, Amy Krans, Caitlin M Rodriguez, Alexander E Linsalata, Aaron C Goldstrohm, Peter K Todd. Mol Cell 2016
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C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking.
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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.