Xiaoqiang Tang, Arturo Toro, Sahana T G, Junli Gao, Jessica Chalk, Björn Oskarsson, Ke Zhang. Mol Neurodegener 2020
Times Cited: 10
Times Cited: 10
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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Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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Mechanisms of Immune Activation by c9orf72-Expansions in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.
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Traffic jam at the nuclear pore: All roads lead to nucleocytoplasmic transport defects in ALS/FTD.
Claudia Fallini, Bilal Khalil, Courtney L Smith, Wilfried Rossoll. Neurobiol Dis 2020
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ALS-associated mutations in TDP-43 increase its stability and promote TDP-43 complexes with FUS/TLS.
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Therapeutic modulation of eIF2α phosphorylation rescues TDP-43 toxicity in amyotrophic lateral sclerosis disease models.
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Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72.
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Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6.
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Comparative interactomics analysis of different ALS-associated proteins identifies converging molecular pathways.
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Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
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ALS-linked TDP-43 mutations produce aberrant RNA splicing and adult-onset motor neuron disease without aggregation or loss of nuclear TDP-43.
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C9orf72 nucleotide repeat structures initiate molecular cascades of disease.
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The C9ORF72 GGGGCC expansion forms RNA G-quadruplex inclusions and sequesters hnRNP H to disrupt splicing in ALS brains.
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Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions.
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TDP-43 is a developmentally regulated protein essential for early embryonic development.
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A C9ORF72/SMCR8-containing complex regulates ULK1 and plays a dual role in autophagy.
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Synaptic localization of C9orf72 regulates post-synaptic glutamate receptor 1 levels.
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Association between repeat sizes and clinical and pathological characteristics in carriers of C9ORF72 repeat expansions (Xpansize-72): a cross-sectional cohort study.
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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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Large C9orf72 hexanucleotide repeat expansions are seen in multiple neurodegenerative syndromes and are more frequent than expected in the UK population.
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C9orf72 suppresses systemic and neural inflammation induced by gut bacteria.
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C9ORF72 interaction with cofilin modulates actin dynamics in motor neurons.
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Amyotrophic lateral sclerosis: update on clinical management.
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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.
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Loss-of-function mutations in the C9ORF72 mouse ortholog cause fatal autoimmune disease.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking.
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C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.
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C9orf72, a protein associated with amyotrophic lateral sclerosis (ALS) is a guanine nucleotide exchange factor.
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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins.
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C9orf72 Dipeptide Repeats Impair the Assembly, Dynamics, and Function of Membrane-Less Organelles.
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ALS Genetics: Gains, Losses, and Implications for Future Therapies.
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Molecular Mechanisms of Neurodegeneration Related to C9orf72 Hexanucleotide Repeat Expansion.
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Cellular and physiological functions of C9ORF72 and implications for ALS/FTD.
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Comparison of parallel high-throughput RNA sequencing between knockout of TDP-43 and its overexpression reveals primarily nonreciprocal and nonoverlapping gene expression changes in the central nervous system of Drosophila.
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Amyotrophic Lateral Sclerosis Modifiers in Drosophila Reveal the Phospholipase D Pathway as a Potential Therapeutic Target.
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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.