318 related articles for article (PubMed ID: 9410897)
21. A novel point mutation (G-1 to T) in a 5' splice donor site of intron 13 of the dystrophin gene results in exon skipping and is responsible for Becker muscular dystrophy.
Hagiwara Y; Nishio H; Kitoh Y; Takeshima Y; Narita N; Wada H; Yokoyama M; Nakamura H; Matsuo M
Am J Hum Genet; 1994 Jan; 54(1):53-61. PubMed ID: 8279470
[TBL] [Abstract][Full Text] [Related]
22. A novel cryptic exon in intron 2 of the human dystrophin gene evolved from an intron by acquiring consensus sequences for splicing at different stages of anthropoid evolution.
Dwi Pramono ZA; Takeshima Y; Surono A; Ishida T; Matsuo M
Biochem Biophys Res Commun; 2000 Jan; 267(1):321-8. PubMed ID: 10623618
[TBL] [Abstract][Full Text] [Related]
23. Two alternative exons can result from activation of the cryptic splice acceptor site deep within intron 2 of the dystrophin gene in a patient with as yet asymptomatic dystrophinopathy.
Yagi M; Takeshima Y; Wada H; Nakamura H; Matsuo M
Hum Genet; 2003 Feb; 112(2):164-70. PubMed ID: 12522557
[TBL] [Abstract][Full Text] [Related]
24. Interplay between exonic splicing enhancers, mRNA processing, and mRNA surveillance in the dystrophic Mdx mouse.
Buvoli M; Buvoli A; Leinwand LA
PLoS One; 2007 May; 2(5):e427. PubMed ID: 17487273
[TBL] [Abstract][Full Text] [Related]
25. [Molecular genetics and problems found in genetic diagnosis of Duchenne Becker muscular dystrophy].
Takeshima Y; Matsuo M
Nihon Rinsho; 1997 Dec; 55(12):3120-5. PubMed ID: 9436421
[TBL] [Abstract][Full Text] [Related]
26. A strong exonic splicing enhancer in dystrophin exon 19 achieve proper splicing without an upstream polypyrimidine tract.
Habara Y; Doshita M; Hirozawa S; Yokono Y; Yagi M; Takeshima Y; Matsuo M
J Biochem; 2008 Mar; 143(3):303-10. PubMed ID: 18039686
[TBL] [Abstract][Full Text] [Related]
27. By-passing the nonsense mutation in the 4 CV mouse model of muscular dystrophy by induced exon skipping.
Mitrpant C; Fletcher S; Iversen PL; Wilton SD
J Gene Med; 2009 Jan; 11(1):46-56. PubMed ID: 19006096
[TBL] [Abstract][Full Text] [Related]
28. A deep intronic mutation in FGB creates a consensus exonic splicing enhancer motif that results in afibrinogenemia caused by aberrant mRNA splicing, which can be corrected in vitro with antisense oligonucleotide treatment.
Davis RL; Homer VM; George PM; Brennan SO
Hum Mutat; 2009 Feb; 30(2):221-7. PubMed ID: 18853456
[TBL] [Abstract][Full Text] [Related]
29. A putative exonic splicing enhancer in exon 7 of the PDHA1 gene affects splicing of adjacent exons.
Ridout CK; Keighley P; Krywawych S; Brown RM; Brown GK
Hum Mutat; 2008 Mar; 29(3):451. PubMed ID: 18273899
[TBL] [Abstract][Full Text] [Related]
30. Skipping of an exon with a nonsense mutation in the DMD gene is induced by the conversion of a splicing enhancer to a splicing silencer.
Zhu Y; Deng H; Chen X; Li H; Yang C; Li S; Pan X; Tian S; Feng S; Tan X; Matsuo M; Zhang Z
Hum Genet; 2019 Jul; 138(7):771-785. PubMed ID: 31168774
[TBL] [Abstract][Full Text] [Related]
31. Improved antisense oligonucleotide induced exon skipping in the mdx mouse model of muscular dystrophy.
Mann CJ; Honeyman K; McClorey G; Fletcher S; Wilton SD
J Gene Med; 2002; 4(6):644-54. PubMed ID: 12439856
[TBL] [Abstract][Full Text] [Related]
32. Multiexon skipping leading to an artificial DMD protein lacking amino acids from exons 45 through 55 could rescue up to 63% of patients with Duchenne muscular dystrophy.
Béroud C; Tuffery-Giraud S; Matsuo M; Hamroun D; Humbertclaude V; Monnier N; Moizard MP; Voelckel MA; Calemard LM; Boisseau P; Blayau M; Philippe C; Cossée M; Pagès M; Rivier F; Danos O; Garcia L; Claustres M
Hum Mutat; 2007 Feb; 28(2):196-202. PubMed ID: 17041910
[TBL] [Abstract][Full Text] [Related]
33. Antisense oligonucleotide-induced exon skipping restores dystrophin expression in vitro in a canine model of DMD.
McClorey G; Moulton HM; Iversen PL; Fletcher S; Wilton SD
Gene Ther; 2006 Oct; 13(19):1373-81. PubMed ID: 16724091
[TBL] [Abstract][Full Text] [Related]
34. Identification of a novel exonic mutation at -13 from 5' splice site causing exon skipping in a girl with mitochondrial acetoacetyl-coenzyme A thiolase deficiency.
Fukao T; Yamaguchi S; Wakazono A; Orii T; Hoganson G; Hashimoto T
J Clin Invest; 1994 Mar; 93(3):1035-41. PubMed ID: 7907600
[TBL] [Abstract][Full Text] [Related]
35. Exon 44 nonsense mutation in two-Duchenne muscular dystrophy brothers detected by heteroduplex analysis.
Prior TW; Papp AC; Snyder PJ; Burghes AH; Sedra MS; Western LM; Bartolo C; Mendell JR
Hum Mutat; 1993; 2(3):192-5. PubMed ID: 8364587
[TBL] [Abstract][Full Text] [Related]
36. A novel cryptic exon in intron 3 of the dystrophin gene was incorporated into dystrophin mRNA with a single nucleotide deletion in exon 5.
Suminaga R; Takeshima Y; Adachi K; Yagi M; Nakamura H; Matsuo M
J Hum Genet; 2002; 47(4):196-201. PubMed ID: 12166656
[TBL] [Abstract][Full Text] [Related]
37. Contemporary retrotransposition of a novel non-coding gene induces exon-skipping in dystrophin mRNA.
Awano H; Malueka RG; Yagi M; Okizuka Y; Takeshima Y; Matsuo M
J Hum Genet; 2010 Dec; 55(12):785-90. PubMed ID: 20827276
[TBL] [Abstract][Full Text] [Related]
38. Chimeric RNA/ethylene-bridged nucleic acids promote dystrophin expression in myocytes of duchenne muscular dystrophy by inducing skipping of the nonsense mutation-encoding exon.
Surono A; Van Khanh T; Takeshima Y; Wada H; Yagi M; Takagi M; Koizumi M; Matsuo M
Hum Gene Ther; 2004 Aug; 15(8):749-57. PubMed ID: 15319032
[TBL] [Abstract][Full Text] [Related]
39. Mutation spectrum leading to an attenuated phenotype in dystrophinopathies.
Tuffery-Giraud S; Saquet C; Thorel D; Disset A; Rivier F; Malcolm S; Claustres M
Eur J Hum Genet; 2005 Dec; 13(12):1254-60. PubMed ID: 16077730
[TBL] [Abstract][Full Text] [Related]
40. Newly recognized exons induced by a splicing abnormality from an intronic mutation of the dystrophin gene resulting in Duchenne muscular dystrophy. Mutations in brief no. 213. Online.
Ikezawa M; Nishino I; Goto Y; Miike T; Nonaka I
Hum Mutat; 1999; 13(2):170. PubMed ID: 10094556
[TBL] [Abstract][Full Text] [Related]
[Previous] [Next] [New Search]
