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Times Cited: 212
Times Cited: 212
Times Cited
Times Co-cited
Similarity
Non-ATG-initiated translation directed by microsatellite expansions.
Tao Zu, Brian Gibbens, Noelle S Doty, Mário Gomes-Pereira, Aline Huguet, Matthew D Stone, Jamie Margolis, Mark Peterson, Todd W Markowski, Melissa A C Ingram,[...]. Proc Natl Acad Sci U S A 2011
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Bidirectional expression of CUG and CAG expansion transcripts and intranuclear polyglutamine inclusions in spinocerebellar ataxia type 8.
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An antisense transcript spanning the CGG repeat region of FMR1 is upregulated in premutation carriers but silenced in full mutation individuals.
Paula D Ladd, Leslie E Smith, Natalia A Rabaia, James M Moore, Sara A Georges, R Scott Hansen, Randi J Hagerman, Flora Tassone, Stephen J Tapscott, Galina N Filippova. Hum Mol Genet 2007
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CTCF-binding sites flank CTG/CAG repeats and form a methylation-sensitive insulator at the DM1 locus.
G N Filippova, C P Thienes, B H Penn, D H Cho, Y J Hu, J M Moore, T R Klesert, V V Lobanenkov, S J Tapscott. Nat Genet 2001
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CTCF regulates ataxin-7 expression through promotion of a convergently transcribed, antisense noncoding RNA.
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Myotonic dystrophy mutation: an unstable CTG repeat in the 3' untranslated region of the gene.
M Mahadevan, C Tsilfidis, L Sabourin, G Shutler, C Amemiya, G Jansen, C Neville, M Narang, J Barceló, K O'Hoy. Science 1992
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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
Mariely DeJesus-Hernandez, Ian R Mackenzie, Bradley F Boeve, Adam L Boxer, Matt Baker, Nicola J Rutherford, Alexandra M Nicholson, NiCole A Finch, Heather Flynn, Jennifer Adamson,[...]. Neuron 2011
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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
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Molecular basis of myotonic dystrophy: expansion of a trinucleotide (CTG) repeat at the 3' end of a transcript encoding a protein kinase family member.
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An antisense CAG repeat transcript at JPH3 locus mediates expanded polyglutamine protein toxicity in Huntington's disease-like 2 mice.
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Myotonic dystrophy type 2 caused by a CCTG expansion in intron 1 of ZNF9.
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Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS.
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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.
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Targeting nuclear RNA for in vivo correction of myotonic dystrophy.
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A natural antisense transcript at the Huntington's disease repeat locus regulates HTT expression.
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RNA gain-of-function in spinocerebellar ataxia type 8.
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Recruitment of human muscleblind proteins to (CUG)(n) expansions associated with myotonic dystrophy.
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Expanded CTG repeat demarcates a boundary for abnormal CpG methylation in myotonic dystrophy patient tissues.
Arturo López Castel, Masayuki Nakamori, Stephanie Tomé, David Chitayat, Geneviève Gourdon, Charles A Thornton, Christopher E Pearson. Hum Mol Genet 2011
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An untranslated CTG expansion causes a novel form of spinocerebellar ataxia (SCA8)
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Myotonic dystrophy in transgenic mice expressing an expanded CUG repeat.
A Mankodi, E Logigian, L Callahan, C McClain, R White, D Henderson, M Krym, C A Thornton. Science 2000
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RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.
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Partners in crime: bidirectional transcription in unstable microsatellite disease.
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Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome.
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A muscleblind knockout model for myotonic dystrophy.
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CGG repeat-associated translation mediates neurodegeneration in fragile X tremor ataxia syndrome.
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An unstable triplet repeat in a gene related to myotonic muscular dystrophy.
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Repeat instability as the basis for human diseases and as a potential target for therapy.
Arturo López Castel, John D Cleary, Christopher E Pearson. Nat Rev Mol Cell Biol 2010
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Transcriptionally Repressive Chromatin Remodelling and CpG Methylation in the Presence of Expanded CTG-Repeats at the DM1 Locus.
Judith Rixt Brouwer, Aline Huguet, Annie Nicole, Arnold Munnich, Geneviève Gourdon. J Nucleic Acids 2013
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Muscleblind localizes to nuclear foci of aberrant RNA in myotonic dystrophy types 1 and 2.
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Myotonic dystrophy type 1 is associated with nuclear foci of mutant RNA, sequestration of muscleblind proteins and deregulated alternative splicing in neurons.
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Trinucleotide repeat expansion at the myotonic dystrophy locus reduces expression of DMAHP.
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Huntington's disease--like 2 is associated with CUG repeat-containing RNA foci.
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RNA toxicity is a component of ataxin-3 degeneration in Drosophila.
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Triplet repeat-derived siRNAs enhance RNA-mediated toxicity in a Drosophila model for myotonic dystrophy.
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Reversal of RNA missplicing and myotonia after muscleblind overexpression in a mouse poly(CUG) model for myotonic dystrophy.
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Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy.
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Mechanisms of trinucleotide repeat instability during human development.
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CTCF cis-regulates trinucleotide repeat instability in an epigenetic manner: a novel basis for mutational hot spot determination.
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Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion.
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The DMPK gene of severely affected myotonic dystrophy patients is hypermethylated proximal to the largely expanded CTG repeat.
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Repeat-associated non-ATG (RAN) translation in neurological disease.
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Spinocerebellar ataxia type 31 is associated with "inserted" penta-nucleotide repeats containing (TGGAA)n.
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Triplet-repeat oligonucleotide-mediated reversal of RNA toxicity in myotonic dystrophy.
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Reversal of RNA dominance by displacement of protein sequestered on triplet repeat RNA.
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Epigenetic silencing in Friedreich ataxia is associated with depletion of CTCF (CCCTC-binding factor) and antisense transcription.
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RAN Translation in Huntington Disease.
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Absence of expression of the FMR-1 gene in fragile X syndrome.
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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.