Induction of revertant fibres in the mdx mouse using antisense oligonucleotides
暂无分享,去创建一个
[1] P. Iversen,et al. Antisense oligonucleotide-induced exon skipping restores dystrophin expression in vitro in a canine model of DMD , 2006, Gene Therapy.
[2] S. Wilton,et al. Dystrophin expression in the mdx mouse after localised and systemic administration of a morpholino antisense oligonucleotide , 2006, The journal of gene medicine.
[3] Ramil N. Nurtdinov,et al. Alternative splicing and protein function , 2005, BMC Bioinformatics.
[4] M. Byrom,et al. Antisense inhibition of human miRNAs and indications for an involvement of miRNA in cell growth and apoptosis , 2005, Nucleic acids research.
[5] J. Morgan,et al. Duchenne's muscular dystrophy: animal models used to investigate pathogenesis and develop therapeutic strategies , 2003, International journal of experimental pathology.
[6] C. Mann,et al. Functional amounts of dystrophin produced by skipping the mutated exon in the mdx dystrophic mouse , 2003, Nature Medicine.
[7] Jinhua Wang,et al. ESEfinder: a web resource to identify exonic splicing enhancers , 2003, Nucleic Acids Res..
[8] C. Mann,et al. Target selection for antisense oligonucleotide induced exon skipping in the dystrophin gene , 2003, The journal of gene medicine.
[9] C. Mann,et al. Improved antisense oligonucleotide induced exon skipping in the mdx mouse model of muscular dystrophy , 2002, The journal of gene medicine.
[10] N. Bresolin,et al. The dystrophin gene is alternatively spliced throughout its coding sequence , 2002, FEBS letters.
[11] F. Baas,et al. Antisense-induced exon skipping restores dystrophin expression in DMD patient derived muscle cells. , 2001, Human molecular genetics.
[12] P. Iversen. Phosphorodiamidate morpholino oligomers: favorable properties for sequence-specific gene inactivation. , 2001, Current opinion in molecular therapeutics.
[13] C. Mann,et al. Antisense-induced exon skipping and synthesis of dystrophin in the mdx mouse. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[14] S. Wilton,et al. Massive Idiosyncratic Exon Skipping Corrects the Nonsense Mutation in Dystrophic Mouse Muscle and Produces Functional Revertant Fibers by Clonal Expansion , 2000, The Journal of cell biology.
[15] J. Summerton. Morpholino antisense oligomers: the case for an RNase H-independent structural type. , 1999, Biochimica et biophysica acta.
[16] S. Agrawal,et al. Specific removal of the nonsense mutation from the mdx dystrophin mRNA using antisense oligonucleotides , 1999, Neuromuscular Disorders.
[17] A. Sadeghi,et al. Redefinition of dystrophin isoform distribution in mouse tissue by RT-PCR implies role in nonmuscle manifestations of duchenne muscular dystrophy. , 1998, Molecular genetics and metabolism.
[18] C. Mann,et al. Alternative dystrophin gene transcripts in golden retriever muscular dystrophy , 1998, Muscle & nerve.
[19] C. Milcarek,et al. Expression of the thyroid hormone receptor gene, erbAalpha, in B lymphocytes: alternative mRNA processing is independent of differentiation but correlates with antisense RNA levels. , 1997, Nucleic acids research.
[20] N. Laing,et al. Revertant fibres: a possible genetic therapy for Duchenne muscular dystrophy? , 1997, Neuromuscular Disorders.
[21] N. Laing,et al. Dystrophin gene transcripts skipping the mdx mutation , 1997, Muscle & nerve.
[22] S. Wilton,et al. Bandstab: a PCR-based alternative to cloning PCR products. , 1997, BioTechniques.
[23] G. Danieli,et al. Duchenne phenotype with in‐frame deletion removing major portion of dystrophin rod: Threshold effect for deletion size? , 1996, Muscle & nerve.
[24] G. Danieli,et al. Dystrophin‐positive fibers in duchenne dystrophy: Origin and correlation to clinical course , 1995, Muscle & nerve.
[25] T. Helliwell,et al. Characterization of revertant muscle fibers in Duchenne muscular dystrophy, using exon-specific monoclonal antibodies against dystrophin. , 1995, American journal of human genetics.
[26] T. Miike,et al. PCR and immunocytochemical analyses of dystrophin-positive fibers in Duchenne muscular dystrophy , 1995, Journal of the Neurological Sciences.
[27] K. Bushby,et al. Becker muscular dystrophy with onset after 60 years , 1994, Neurology.
[28] Y. Takeshima,et al. Amino‐terminal deletion of 53% of dystrophin results in an intermediate Duchenne‐Becker muscular dystrophy phenotype , 1994, Neurology.
[29] M. Passos-Bueno,et al. Half the dystrophin gene is apparently enough for a mild clinical course: confirmation of its potential use for gene therapy. , 1994, Human molecular genetics.
[30] M. Noble,et al. Myogenic cell lines derived from transgenic mice carrying a thermolabile T antigen: a model system for the derivation of tissue-specific and mutation-specific cell lines. , 1994, Developmental biology.
[31] K. Davies,et al. Dystrophin and dystrophin-related proteins: A review of protein and RNA studies , 1993, Neuromuscular Disorders.
[32] F. Muntoni,et al. Muscular weakness in the mdx mouse , 1993, Journal of the Neurological Sciences.
[33] T. Vulliamy,et al. Exon skipping and translation in patients with frameshift deletions in the dystrophin gene. , 1993, American journal of human genetics.
[34] K. Bushby,et al. Integrated study of 100 patients with Xp21 linked muscular dystrophy using clinical, genetic, immunochemical, and histopathological data. Part 3. Differential diagnosis and prognosis. , 1993, Journal of medical genetics.
[35] L. Kunkel,et al. The structural and functional diversity of dystrophin , 1993, Nature Genetics.
[36] D. Libri,et al. Pre‐mRNA secondary structure and the regulation of splicing , 1993, BioEssays : news and reviews in molecular, cellular and developmental biology.
[37] V. Chapman,et al. The Frequency of Revertants in mdx Mouse Genetic Models for Duchenne Muscular Dystrophy , 1992, Pediatric Research.
[38] R. Bartlett,et al. An error in dystrophin mRNA processing in golden retriever muscular dystrophy, an animal homologue of Duchenne muscular dystrophy. , 1992, Genomics.
[39] J. Mendell,et al. Somatic reversion/suppression in Duchenne muscular dystrophy (DMD): evidence supporting a frame-restoring mechanism in rare dystrophin-positive fibers. , 1992, American journal of human genetics.
[40] R Kole,et al. Selection of splice sites in pre-mRNAs with short internal exons , 1991, Molecular and cellular biology.
[41] H Sugita,et al. Exploring the molecular basis for variability among patients with Becker muscular dystrophy: dystrophin gene and protein studies. , 1991, American journal of human genetics.
[42] J. Mendell,et al. Dystrophin expression and somatic reversion in prednisone‐treated and untreated Duchenne dystrophy , 1991, Neurology.
[43] Simon C Watkins,et al. Somatic reversion/suppression of the mouse mdx phenotype in vivo , 1990, Journal of the Neurological Sciences.
[44] K. Davies,et al. Very mild muscular dystrophy associated with the deletion of 46% of dystrophin , 1990, Nature.
[45] Marvin B. Shapiro,et al. RNA splice junctions of different classes of eukaryotes: sequence statistics and functional implications in gene expression. , 1987, Nucleic acids research.
[46] K. Moore,et al. X chromosome-linked muscular dystrophy (mdx) in the mouse. , 1984, Proceedings of the National Academy of Sciences of the United States of America.
[47] G. van Ommen,et al. Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense. , 2004, American journal of human genetics.
[48] G. van Ommen,et al. Advances in Duchenne muscular dystrophy gene therapy , 2003, Nature reviews. Genetics.
[49] A. J. Lopez,et al. Alternative splicing of pre-mRNA: developmental consequences and mechanisms of regulation. , 1998, Annual review of genetics.
[50] W. King,et al. Characterization of translational frame exception patients in Duchenne/Becker muscular dystrophy. , 1993, Human molecular genetics.
[51] A. Monaco,et al. An explanation for the phenotypic differences between patients bearing partial deletions of the DMD locus. , 1988, Genomics.
[52] Eric P. Hoffman,et al. Dystrophin: The protein product of the duchenne muscular dystrophy locus , 1987, Cell.