Steve D. Wilton mainly focuses on Dystrophin, Molecular biology, Exon skipping, Duchenne muscular dystrophy and Genetics. His Dystrophin research includes elements of Phenotype and RNA splicing. His studies deal with areas such as Transcription factor, DUX4, Facioscapulohumeral muscular dystrophy, Small interfering RNA and RNA interference as well as Molecular biology.
His Exon skipping study deals with the bigger picture of Exon. His work carried out in the field of Duchenne muscular dystrophy brings together such families of science as Eteplirsen, In vivo and Morpholino. His work on Nemaline myopathy, Point mutation, Gene and Autosome is typically connected to Nemaline bodies as part of general Genetics study, connecting several disciplines of science.
The scientist’s investigation covers issues in Exon, Dystrophin, Molecular biology, Duchenne muscular dystrophy and Exon skipping. His Exon research integrates issues from RNA splicing, Morpholino and splice. His research in Dystrophin intersects with topics in In vivo and Cell biology.
His work deals with themes such as Splice site mutation, Transfection, Gene mapping and Skeletal muscle, which intersect with Molecular biology. His work in Duchenne muscular dystrophy covers topics such as Bioinformatics which are related to areas like Disease. The various areas that he examines in his Exon skipping study include Nonsense mutation, Exon trapping and Gene duplication, Tandem exon duplication.
His primary areas of study are Exon, RNA splicing, Exon skipping, Molecular biology and splice. His Exon research incorporates elements of Duchenne muscular dystrophy, Dystrophin and Morpholino. His RNA splicing research is multidisciplinary, relying on both Cancer research, Mutation, Cystic fibrosis, Computational biology and Intron.
Steve D. Wilton combines subjects such as Glutamine and Spinocerebellar ataxia with his study of Exon skipping. His Molecular biology research is multidisciplinary, incorporating elements of Transfection and Spliceosome. The splice study combines topics in areas such as Collagen VI and Muscular dystrophy.
Steve D. Wilton focuses on Exon, RNA splicing, Cell biology, Alternative splicing and Morpholino. Steve D. Wilton is interested in Exon skipping, which is a branch of Exon. His studies in Exon skipping integrate themes in fields like Phosphorothioate Oligonucleotides, Duchenne muscular dystrophy and Spinocerebellar ataxia.
The study incorporates disciplines such as Cancer research, Computational biology and Oligonucleotide in addition to RNA splicing. His research integrates issues of Glutamine, Transfection and Hedgehog signaling pathway in his study of Cell biology. His Morpholino research is multidisciplinary, incorporating perspectives in Electroporation and Ataxin.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Exon skipping and dystrophin restoration in patients with Duchenne muscular dystrophy after systemic phosphorodiamidate morpholino oligomer treatment: an open-label, phase 2, dose-escalation study.
Sebahattin Cirak;Virginia Arechavala-Gomeza;Michela Guglieri;Lucy Feng.
The Lancet (2011)
Local restoration of dystrophin expression with the morpholino oligomer AVI-4658 in Duchenne muscular dystrophy: a single-blind, placebo-controlled, dose-escalation, proof-of-concept study
Maria Kinali;Maria Kinali;Virginia Arechavala-Gomeza;Lucy Feng;Sebahattin Cirak.
Lancet Neurology (2009)
Systemic delivery of morpholino oligonucleotide restores dystrophin expression bodywide and improves dystrophic pathology
Julia Alter;Fang Lou;Adam Rabinowitz;HaiFang Yin.
Nature Medicine (2006)
Regulation of eukaryotic gene expression by the untranslated gene regions and other non-coding elements
Lucy W. Barrett;Sue Fletcher;Steve D. Wilton.
Cellular and Molecular Life Sciences (2012)
A mutation in the alpha tropomyosin gene TPM3 associated with autosomal dominant nemaline myopathy.
Laing Ng;Wilton Sd;Akkari Pa;Akkari Pa;Dorosz S.
Nature Genetics (1995)
Antisense oligonucleotide-induced exon skipping across the human dystrophin gene transcript.
Steve D Wilton;Abbie M Fall;Penny L Harding;Graham McClorey.
Molecular Therapy (2007)
Antisense oligonucleotide-induced exon skipping restores dystrophin expression in vitro in a canine model of DMD
Graham Mcclorey;H.M. Moulton;P.L. Iversen;Susan Fletcher.
Gene Therapy (2006)
Detection and Identification of Multiple Mycobacterial Pathogens by DNA Amplification in a Single Tube
Steve Wilton;Debby Cousins.
Genome Research (1992)
ALS Genetics, Mechanisms, and Therapeutics: Where Are We Now?
Rita Mejzini;Loren Louise Flynn;Loren Louise Flynn;Ianthe Leigh Pitout;Ianthe Leigh Pitout;Sue Fletcher;Sue Fletcher.
Frontiers in Neuroscience (2019)
Massive idiosyncratic exon skipping corrects the nonsense mutation in dystrophic mouse muscle and produces functional revertant fibers by clonal expansion.
Q.L. Lu;G.E. Morris;Steve Wilton;T. Ly.
Journal of Cell Biology (2000)
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