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Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
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The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.
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Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations.
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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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TDP-43 is intrinsically aggregation-prone, and amyotrophic lateral sclerosis-linked mutations accelerate aggregation and increase toxicity.
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Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways.
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A Liquid-to-Solid Phase Transition of the ALS Protein FUS Accelerated by Disease Mutation.
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TDP-43 A315T mutation in familial motor neuron disease.
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ALS Genetics, Mechanisms, and Therapeutics: Where Are We Now?
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Exome sequencing reveals VCP mutations as a cause of familial ALS.
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TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD.
Jonathan P Ling, Olga Pletnikova, Juan C Troncoso, Philip C Wong. Science 2015
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Characterizing the RNA targets and position-dependent splicing regulation by TDP-43.
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Structural determinants of the cellular localization and shuttling of TDP-43.
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Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis.
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Protein aggregation in amyotrophic lateral sclerosis.
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Anna M Blokhuis, Ewout J N Groen, Max Koppers, Leonard H van den Berg, R Jeroen Pasterkamp. Acta Neuropathol 2013
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Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia.
Axel Freischmidt, Thomas Wieland, Benjamin Richter, Wolfgang Ruf, Veronique Schaeffer, Kathrin Müller, Nicolai Marroquin, Frida Nordin, Annemarie Hübers, Patrick Weydt,[...]. Nat Neurosci 2015
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GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.
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SQSTM1 mutations in familial and sporadic amyotrophic lateral sclerosis.
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Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia.
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TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD.
Ching-Chieh Chou, Yi Zhang, Mfon E Umoh, Spencer W Vaughan, Ileana Lorenzini, Feilin Liu, Melissa Sayegh, Paul G Donlin-Asp, Yu Han Chen, Duc M Duong,[...]. Nat Neurosci 2018
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Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
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9
Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits, and early mortality in transgenic mice.
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ALS Genetics: Gains, Losses, and Implications for Future Therapies.
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12
Axonal transport of TDP-43 mRNA granules is impaired by ALS-causing mutations.
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ALS Mutations Disrupt Phase Separation Mediated by α-Helical Structure in the TDP-43 Low-Complexity C-Terminal Domain.
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TDP-43 regulates its mRNA levels through a negative feedback loop.
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Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death.
Fatima Gasset-Rosa, Shan Lu, Haiyang Yu, Cong Chen, Ze'ev Melamed, Lin Guo, James Shorter, Sandrine Da Cruz, Don W Cleveland. Neuron 2019
Fatima Gasset-Rosa, Shan Lu, Haiyang Yu, Cong Chen, Ze'ev Melamed, Lin Guo, James Shorter, Sandrine Da Cruz, Don W Cleveland. Neuron 2019
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ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import.
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Phase separation by low complexity domains promotes stress granule assembly and drives pathological fibrillization.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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C9orf72 Dipeptide Repeats Impair the Assembly, Dynamics, and Function of Membrane-Less Organelles.
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ER-mitochondria associations are regulated by the VAPB-PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43.
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8
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.