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Exon-Skipping Oligonucleotides Restore Functional Collagen VI by Correcting a Common COL6A1 Mutation in Ullrich CMD
Aguti S, Aguti S, Bolduc V, et al.
Molecular therapy. Nucleic acids, 2020, 21, p 205
Myostatin inhibition in combination with antisense oligonucleotide therapy improves outcomes in spinal muscular atrophy
Zhou H, Meng J, Malerba A, et al.
Journal of cachexia, sarcopenia and muscle, 2020
Cardiac Phenotype-Genotype Associations in DMD/BMD: A Meta-Analysis and Systematic Review
Zhou H
2020
The authors reply: Letter on: "Myostatin inhibition in combination with antisense oligonucleotide therapy improves outcomes in spinal muscular atrophy" by Zhou et al
Zhou H, Muntoni F
Journal of cachexia, sarcopenia and muscle, 2020
Gapmer Antisense Oligonucleotides to Selectively Suppress the Mutant Allele in COL6A Genes in Dominant Ullrich Congenital Muscular Dystrophy
Aguti S, Marrosu E, Muntoni F, et al.
Methods in molecular biology (Clifton, N.J.), 2020, 2176, p 221
A recurrent COL6A1 pseudoexon insertion causes muscular dystrophy and is effectively targeted by splice-correction therapies
Bolduc V, Foley AR, Solomon-Degefa H, et al.
JCI insight, 2019, 4, 6
The progress of AAV-mediated gene therapy in neuromuscular disorders
Aguti S, Malerba A, Zhou H
Expert opinion on biological therapy, 2018, 18, 6, p 681
Gapmer Antisense Oligonucleotides Suppress the Mutant Allele of COL6A3 and Restore Functional Protein in Ullrich Muscular Dystrophy
Marrosu E, Ala P, Muntoni F, et al.
Molecular therapy. Nucleic acids, 2017, 8, p 416
Antisense Oligonucleotide-Based Therapy for Neuromuscular Disease
Sardone V, Zhou H, Muntoni F, et al.
Molecules (Basel, Switzerland), 2017, 22, 4
Tacrolimus in the treatment of myasthenia gravis in patients with an inadequate response to glucocorticoid therapy: randomized, double-blind, placebo-controlled study conducted in China
Zhou L, Liu W, Li W, et al.
Therapeutic advances in neurological disorders, 2017, 10, 9, p 315
Infantile spinal muscular atrophy with respiratory distress type I presenting without respiratory involvement: Novel mutations and review of the literature
Luan X, Huang X, Liu X, et al.
Brain & development, 2016, 38, 7, p 685
MiR-15a contributes abnormal immune response in myasthenia gravis by targeting CXCL10
Liu XF, Wang RQ, Hu B, et al.
Clinical immunology, 2016, 164, p 106
Altered Levels of MicroRNA-9, -206, and -132 in Spinal Muscular Atrophy and Their Response to Antisense Oligonucleotide Therapy
Catapano F, Zaharieva I, Scoto M, et al.
Molecular therapy. Nucleic acids, 2016, 5, 7
Systemic peptide-mediated oligonucleotide therapy improves long-term survival in spinal muscular atrophy
Hammond SM, Hazell G, Shabanpoor F, et al.
Proceedings of the national Academy of sciences of the United States of America, 2016, 113, 39, p 10962
Survival Motor Neuron (SMN) protein is required for normal mouse liver development
Szunyogova E, Zhou H, Maxwell GK, et al.
Scientific Reports, 2016, 6
Repeated low doses of morpholino antisense oligomer: an intermediate mouse model of spinal muscular atrophy to explore the window of therapeutic response
Zhou H, Meng J, Marrosu E, et al.
Human molecular genetics, 2015, 24, 22, p 6265
CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase
He W, Bai G, Zhou H, et al.
Nature, 2015, 526, 7575, p 710
A novel morpholino oligomer targeting ISS-N1 improves rescue of severe SMA transgenic mice
Zhou H, Janghra N, Mitrpant C, et al.
Human gene therapy, 2013, 24, 3, p. 331-342
RyR1 deficiency in congenital myopathies disrupts excitation-contraction coupling
Zhou H, Rokach O, Feng L, et al.
Human mutation, 2013, 34, 7, p 986
Improved antisense oligonucleotide design to suppress aberrant SMN2 gene transcript processing: towards a treatment for spinal muscular atrophy
Mitrpant C, Porensky P, Zhou H, et al.
PLoS ONE, 2013, 8, 4, e62114, 10 p.
Establishment of a human skeletal muscle-derived cell line: biochemical, cellular and electrophysiological characterization
Rokach O, Ullrich ND, Rausch M, et al.
The Biochemical journal, 2013, 455, 2, p 169
Clinical and genetic findings in a large cohort of patients with ryanodine receptor 1 gene-associated myopathies
Klein A, Lillis S, Munteanu I, et al.
Human mutation, 2012, 33, 6, p. 981-988
Mutations in ISPD cause Walker-Warburg syndrome and defective glycosylation of alpha-dystroglycan
Roscioli T, Kamsteeg EJ, Buysse K, et al.
Nature genetics, 2012, Epub 2012/04/24
RYR1 mutations are a common cause of congenital myopathies with central nuclei
Wilmshurst JM, Lillis S, Zhou H, et al.
Annals of neurology, 2010, 68, 5, p. 717-726
Oxidative stress in SEPN1-related myopathy : from pathophysiology to treatment
Arbogast S, Beuvin M, Fraysse B, et al.
Annals of neurology, 2009, 65, 6, p. 677-686
