BIOMARKERS

Molecular Biopsy of Human Tumors

- a resource for Precision Medicine *

574 related articles for article (PubMed ID: 26152642)

  • 1. Neuronal SH-SY5Y cells use the C-dystrophin promoter coupled with exon 78 skipping and display multiple patterns of alternative splicing including two intronic insertion events.
    Nishida A; Minegishi M; Takeuchi A; Awano H; Niba ET; Matsuo M
    Hum Genet; 2015 Sep; 134(9):993-1001. PubMed ID: 26152642
    [TBL] [Abstract][Full Text] [Related]  

  • 2. In vitro splicing analysis showed that availability of a cryptic splice site is not a determinant for alternative splicing patterns caused by +1G-->A mutations in introns of the dystrophin gene.
    Habara Y; Takeshima Y; Awano H; Okizuka Y; Zhang Z; Saiki K; Yagi M; Matsuo M
    J Med Genet; 2009 Aug; 46(8):542-7. PubMed ID: 19001018
    [TBL] [Abstract][Full Text] [Related]  

  • 3. A novel cryptic exon identified in the 3' region of intron 2 of the human dystrophin gene.
    Tran VK; Zhang Z; Yagi M; Nishiyama A; Habara Y; Takeshima Y; Matsuo M
    J Hum Genet; 2005; 50(8):425-433. PubMed ID: 16133659
    [TBL] [Abstract][Full Text] [Related]  

  • 4. Insertion of a 5' truncated L1 element into the 3' end of exon 44 of the dystrophin gene resulted in skipping of the exon during splicing in a case of Duchenne muscular dystrophy.
    Narita N; Nishio H; Kitoh Y; Ishikawa Y; Ishikawa Y; Minami R; Nakamura H; Matsuo M
    J Clin Invest; 1993 May; 91(5):1862-7. PubMed ID: 8387534
    [TBL] [Abstract][Full Text] [Related]  

  • 5. Pseudoexon activation in the DMD gene as a novel mechanism for Becker muscular dystrophy.
    Tuffery-Giraud S; Saquet C; Chambert S; Claustres M
    Hum Mutat; 2003 Jun; 21(6):608-14. PubMed ID: 12754707
    [TBL] [Abstract][Full Text] [Related]  

  • 6. Molecular characterization of the 5'-UTR of retinal dystrophin reveals a cryptic intron that regulates translational activity.
    Kubokawa I; Takeshima Y; Ota M; Enomoto M; Okizuka Y; Mori T; Nishimura N; Awano H; Yagi M; Matsuo M
    Mol Vis; 2010 Dec; 16():2590-7. PubMed ID: 21151598
    [TBL] [Abstract][Full Text] [Related]  

  • 7. Novel cryptic exons identified in introns 2 and 3 of the human dystrophin gene with duplication of exons 8-11.
    Ishibashi K; Takeshima Y; Yagi M; Nishiyama A; Matsuo M
    Kobe J Med Sci; 2006; 52(3-4):61-75. PubMed ID: 16849873
    [TBL] [Abstract][Full Text] [Related]  

  • 8. Cryptic splice activation but not exon skipping is observed in minigene assays of dystrophin c.9361+1G>A mutation identified by NGS.
    Niba ETE; Nishida A; Tran VK; Vu DC; Matsumoto M; Awano H; Lee T; Takeshima Y; Nishio H; Matsuo M
    J Hum Genet; 2017 Apr; 62(5):531-537. PubMed ID: 28100912
    [TBL] [Abstract][Full Text] [Related]  

  • 9. A G-to-A transition at the fifth position of intron-32 of the dystrophin gene inactivates a splice-donor site both in vivo and in vitro.
    Thi Tran HT; Takeshima Y; Surono A; Yagi M; Wada H; Matsuo M
    Mol Genet Metab; 2005 Jul; 85(3):213-9. PubMed ID: 15979033
    [TBL] [Abstract][Full Text] [Related]  

  • 10. Endogenous Multiple Exon Skipping and Back-Splicing at the DMD Mutation Hotspot.
    Suzuki H; Aoki Y; Kameyama T; Saito T; Masuda S; Tanihata J; Nagata T; Mayeda A; Takeda S; Tsukahara T
    Int J Mol Sci; 2016 Oct; 17(10):. PubMed ID: 27754374
    [TBL] [Abstract][Full Text] [Related]  

  • 11. A G-to-T transversion at the splice acceptor site of dystrophin exon 14 shows multiple splicing outcomes that are not exemplified by transition mutations.
    Ota M; Takeshima Y; Nishida A; Awano H; Lee T; Yagi M; Matsuo M
    Genet Test Mol Biomarkers; 2012 Jan; 16(1):3-8. PubMed ID: 21854195
    [TBL] [Abstract][Full Text] [Related]  

  • 12. Splicing analysis disclosed a determinant single nucleotide for exon skipping caused by a novel intraexonic four-nucleotide deletion in the dystrophin gene.
    Tran VK; Takeshima Y; Zhang Z; Yagi M; Nishiyama A; Habara Y; Matsuo M
    J Med Genet; 2006 Dec; 43(12):924-30. PubMed ID: 16738009
    [TBL] [Abstract][Full Text] [Related]  

  • 13. A novel splicing silencer generated by DMD exon 45 deletion junction could explain upstream exon 44 skipping that modifies dystrophinopathy.
    Dwianingsih EK; Malueka RG; Nishida A; Itoh K; Lee T; Yagi M; Iijima K; Takeshima Y; Matsuo M
    J Hum Genet; 2014 Aug; 59(8):423-9. PubMed ID: 24871807
    [TBL] [Abstract][Full Text] [Related]  

  • 14. Identification of seven novel cryptic exons embedded in the dystrophin gene and characterization of 14 cryptic dystrophin exons.
    Zhang Z; Habara Y; Nishiyama A; Oyazato Y; Yagi M; Takeshima Y; Matsuo M
    J Hum Genet; 2007; 52(7):607-617. PubMed ID: 17579806
    [TBL] [Abstract][Full Text] [Related]  

  • 15. 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]  

  • 16. Towards a therapeutic inhibition of dystrophin exon 23 splicing in mdx mouse muscle induced by antisense oligoribonucleotides (splicomers): target sequence optimisation using oligonucleotide arrays.
    Graham IR; Hill VJ; Manoharan M; Inamati GB; Dickson G
    J Gene Med; 2004 Oct; 6(10):1149-58. PubMed ID: 15386737
    [TBL] [Abstract][Full Text] [Related]  

  • 17. 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]  

  • 18. 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]  

  • 19. Becker muscular dystrophy caused by an intronic mutation reducing the efficiency of the splice donor site of intron 26 of the dystrophin gene.
    Baskin B; Banwell B; Khater RA; Hawkins C; Ray PN
    Neuromuscul Disord; 2009 Mar; 19(3):189-92. PubMed ID: 19230662
    [TBL] [Abstract][Full Text] [Related]  

  • 20. Point mutations in the dystrophin gene: evidence for frequent use of cryptic splice sites as a result of splicing defects.
    Tuffery-Giraud S; Chambert S; Demaille J; Claustres M
    Hum Mutat; 1999; 14(5):359-68. PubMed ID: 10533061
    [TBL] [Abstract][Full Text] [Related]  

    [Next]    [New Search]
    of 29.