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Author Details

Helene Tran
2008
16
12
PMIDPaper TitleJournal TitlePublished Year
34949835Suppression of mutant C9orf72 expression by a potent mixed backbone antisense oligonucleotide.Nature Medicine2022
35276083Excessive release of inorganic polyphosphate by ALS/FTD astrocytes causes non-cell-autonomous toxicity to motoneurons.Neuron2022
35145256Reversal of RNA toxicity in myotonic dystrophy via a decoy RNA-binding protein with high affinity for expanded CUG repeats.Nature Biomedical Engineering2022
33558503Variant-selective stereopure oligonucleotides protect against pathologies associated with C9orf72-repeat expansion in preclinical models.Nature Communications2021
32096040Myotonic Dystrophy: an RNA Toxic Gain of Function Tauopathy?Advances in Experimental Medicine and Biology2019
28379367A Drosophila model of ALS reveals a partial loss of function of causative human PFN1 mutants.Human Molecular Genetics2017
27720481Poly(GR) in C9ORF72-Related ALS/FTD Compromises Mitochondrial Function and Increases Oxidative Stress and DNA Damage in iPSC-Derived Motor Neurons.Neuron2016
26637797Human C9ORF72 Hexanucleotide Expansion Reproduces RNA Foci and Dipeptide Repeat Proteins but Not Neurodegeneration in BAC Transgenic Mice.Neuron2015
26402604Differential Toxicity of Nuclear RNA Foci versus Dipeptide Repeat Proteins in a Drosophila Model of C9ORF72 FTD/ALS.Neuron2015
24747743Consensus brain-derived protein, extraction protocol for the study of human and murine brain proteome using both 2D-DIGE and mini 2DE immunoblotting.Journal of Visualized Experiments2014
24409116Brain pathology in myotonic dystrophy: when tauopathy meets spliceopathy and RNAopathy.Frontiers in Molecular Neuroscience2014
23836290Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons.Acta Neuropathol2013
21454535Analysis of exonic regions involved in nuclear localization, splicing activity, and dimerization of Muscleblind-like-1 isoforms.Journal of Biological Chemistry2011
21439371Mis-splicing of Tau exon 10 in myotonic dystrophy type 1 is reproduced by overexpression of CELF2 but not by MBNL1 silencing.2011
19166838Altered splicing of Tau in DM1 is different from the foetal splicing process.FEBS Letters2009
18177861Overexpression of MBNL1 fetal isoforms and modified splicing of Tau in the DM1 brain: two individual consequences of CUG trinucleotide repeats.Experimental Neurology2008
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