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Targeted Antisense Oligonucleotide-Mediated Skipping of Murine Postn Exon 17 Partially Addresses Fibrosis in D2.mdx Mice

International journal of molecular sciences, 2024-06, Vol.25 (11), p.6113

2024

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Microdystrophin Gene Addition Significantly Improves Muscle Functionality and Diaphragm Muscle Histopathology in a Fibrotic Mouse Model of Duchenne Muscular Dystrophy

International journal of molecular sciences, 2023-05, Vol.24 (9), p.8174

2023

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Functional Rescue of Dystrophin Deficiency in Mice Caused by Frameshift Mutations Using Campylobacter jejuni Cas9

Molecular therapy, 2018-06, Vol.26 (6), p.1529-1538

2018

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Genetic therapeutic approaches for Duchenne muscular dystrophy

Human gene therapy, 2012-07, Vol.23 (7), p.676

2012

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Editorial of the Special Issue: Antisense Therapies

Biomedicines, 2018-09, Vol.6 (4), p.95

Popplewell, Linda J

2018

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Knockdown of Muscle-Specific Ribosomal Protein L3-Like Enhances Muscle Function in Healthy and Dystrophic Mice

Nucleic acid therapeutics, 2021-12, Vol.31 (6), p.457

2021

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Design of Phosphorodiamidate Morpholino Oligomers (PMOs) for the Induction of Exon Skipping of the Human DMD Gene

Molecular therapy, 2009-03, Vol.17 (3), p.554-561

2009

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RAC1B modulates intestinal tumourigenesis via modulation of WNT and EGFR signalling pathways

Nature communications, 2021-04, Vol.12 (1), p.2335-17, Article 2335

2021

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Functional muscle recovery following dystrophin and myostatin exon splice modulation in aged mdx mice

Human molecular genetics, 2019-09, Vol.28 (18), p.3091-3100

2019

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Inhibition of Myostatin Reduces Collagen Deposition in a Mouse Model of Oculopharyngeal Muscular Dystrophy (OPMD) With Established Disease

Frontiers in physiology, 2020-03, Vol.11, p.184-184

2020

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Long-Term Systemic Treatment of a Mouse Model Displaying Chronic FSHD-like Pathology with Antisense Therapeutics That Inhibit DUX4 Expression

Biomedicines, 2022-07, Vol.10 (7), p.1623

2022

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Expression of the Pro-Fibrotic Marker Periostin in a Mouse Model of Duchenne Muscular Dystrophy

Biomedicines, 2024-01, Vol.12 (1), p.216

2024

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Optimized lentiviral vector to restore full-length dystrophin via a cell-mediated approach in a mouse model of Duchenne muscular dystrophy

Molecular therapy. Methods & clinical development, 2022-06, Vol.25, p.491-507

2022

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Antisense-induced Myostatin Exon Skipping Leads to Muscle Hypertrophy in Mice Following Octa guanidine Morpholino Oligomer Treatment

Molecular therapy, 2011-01, Vol.19 (1), p.159-164

2011

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Inhibition of myostatin improves muscle atrophy in oculopharyngeal muscular dystrophy (OPMD)

Journal of cachexia, sarcopenia and muscle, 2019-10, Vol.10 (5), p.1016-1026

2019

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Nuclear poly(A)-binding protein aggregates misplace a pre-mRNA outside of SC35 speckle causing its abnormal splicing

Nucleic acids research, 2016-12, Vol.44 (22), p.10929

2016

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The administration of antisense oligonucleotide golodirsen reduces pathological regeneration in patients with Duchenne muscular dystrophy

Acta neuropathologica communications, 2021-01, Vol.9 (1), p.7-7, Article 7

2021

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Systemic Antisense Therapeutics for Dystrophin and Myostatin Exon Splice Modulation Improve Muscle Pathology of Adult mdx Mice

Molecular therapy. Nucleic acids, 2017-03, Vol.6, p.15-28

2017

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Targeting TGFβ Signaling to Address Fibrosis Using Antisense Oligonucleotides

Biomedicines, 2018-06, Vol.6 (3), p.74

2018

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Gene correction of a duchenne muscular dystrophy mutation by meganuclease-enhanced exon knock-in

Human gene therapy, 2013-07, Vol.24 (7), p.692

2013

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Targeted exon skipping of NF1 exon 17 as a therapeutic for neurofibromatosis type I

Molecular therapy. Nucleic acids, 2022-06, Vol.28, p.261-278

2022

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Mutation-Directed Therapeutics for Neurofibromatosis Type I

Molecular therapy. Nucleic acids, 2020-06, Vol.20, p.739-753

2020

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Targeted Antisense Oligonucleotide-Mediated Skipping of Murine Postn Exon 17 Partially Addresses Fibrosis in D2.mdx Mice

Microdystrophin Gene Addition Significantly Improves Muscle Functionality and Diaphragm Muscle Histopathology in a Fibrotic Mouse Model of Duchenne Muscular Dystrophy

Functional Rescue of Dystrophin Deficiency in Mice Caused by Frameshift Mutations Using Campylobacter jejuni Cas9

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

Genetic therapeutic approaches for Duchenne muscular dystrophy

Editorial of the Special Issue: Antisense Therapies

Knockdown of Muscle-Specific Ribosomal Protein L3-Like Enhances Muscle Function in Healthy and Dystrophic Mice

Design of Phosphorodiamidate Morpholino Oligomers (PMOs) for the Induction of Exon Skipping of the Human DMD Gene

RAC1B modulates intestinal tumourigenesis via modulation of WNT and EGFR signalling pathways

Functional muscle recovery following dystrophin and myostatin exon splice modulation in aged mdx mice

Inhibition of Myostatin Reduces Collagen Deposition in a Mouse Model of Oculopharyngeal Muscular Dystrophy (OPMD) With Established Disease

Long-Term Systemic Treatment of a Mouse Model Displaying Chronic FSHD-like Pathology with Antisense Therapeutics That Inhibit DUX4 Expression

Expression of the Pro-Fibrotic Marker Periostin in a Mouse Model of Duchenne Muscular Dystrophy

Optimized lentiviral vector to restore full-length dystrophin via a cell-mediated approach in a mouse model of Duchenne muscular dystrophy

Antisense-induced Myostatin Exon Skipping Leads to Muscle Hypertrophy in Mice Following Octa guanidine Morpholino Oligomer Treatment

Inhibition of myostatin improves muscle atrophy in oculopharyngeal muscular dystrophy (OPMD)

Nuclear poly(A)-binding protein aggregates misplace a pre-mRNA outside of SC35 speckle causing its abnormal splicing

The administration of antisense oligonucleotide golodirsen reduces pathological regeneration in patients with Duchenne muscular dystrophy

A multicenter comparison of quantification methods for antisense oligonucleotide-induced DMD exon 51 skipping in Duchenne muscular dystrophy cell cultures

Systemic Antisense Therapeutics for Dystrophin and Myostatin Exon Splice Modulation Improve Muscle Pathology of Adult mdx Mice

Targeting TGFβ Signaling to Address Fibrosis Using Antisense Oligonucleotides

Reversible immortalisation enables genetic correction of human muscle progenitors and engineering of next‐generation human artificial chromosomes for Duchenne muscular dystrophy

Gene correction of a duchenne muscular dystrophy mutation by meganuclease-enhanced exon knock-in

Targeted exon skipping of NF1 exon 17 as a therapeutic for neurofibromatosis type I

Mutation-Directed Therapeutics for Neurofibromatosis Type I

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