Gene selective suppression of nonsense termination using antisense agents.

[1]  S. R. Kushner,et al.  mRNA Decay in Prokaryotes and Eukaryotes: Different Approaches to a Similar Problem , 2004, IUBMB life.

[2]  J. F. Atkins,et al.  Efficient stimulation of site-specific ribosome frameshifting by antisense oligonucleotides. , 2004, RNA.

[3]  J. Rousset,et al.  Premature stop codons involved in muscular dystrophies show a broad spectrum of readthrough efficiencies in response to gentamicin treatment , 2004, Gene Therapy.

[4]  Isabelle Hatin,et al.  The major 5' determinant in stop codon read-through involves two adjacent adenines. , 2004, Nucleic acids research.

[5]  B. Kerem,et al.  Gentamicin-induced correction of CFTR function in patients with cystic fibrosis and CFTR stop mutations. , 2003, The New England journal of medicine.

[6]  V. Ramakrishnan,et al.  Insights into the decoding mechanism from recent ribosome structures. , 2003, Trends in biochemical sciences.

[7]  G. Piluso,et al.  Gentamicin administration in Duchenne patients with premature stop codon. Preliminary results. , 2003, Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology.

[8]  Yoshikazu Nakamura,et al.  Making sense of mimic in translation termination. , 2003, Trends in biochemical sciences.

[9]  M. Ehrenberg,et al.  Termination of translation: interplay of mRNA, rRNAs and release factors? , 2003, The EMBO journal.

[10]  Jill K Thompson,et al.  The protein synthesis inhibitors, oxazolidinones and chloramphenicol, cause extensive translational inaccuracy in vivo. , 2002, Journal of molecular biology.

[11]  P. Sieving,et al.  X-linked recessive atrophic macular degeneration from RPGR mutation. , 2002, Genomics.

[12]  M. Strazzabosco,et al.  Correction of CFTR malfunction and stimulation of Ca2+‐activated Cl− channels restore HCO  3− secretion in cystic fibrosis bile ductular cells , 2002, Hepatology.

[13]  Y. Takeshima,et al.  Oligonucleotides against a splicing enhancer sequence led to dystrophin production in muscle cells from a Duchenne muscular dystrophy patient , 2001, Brain and Development.

[14]  F. Baas,et al.  Antisense-induced exon skipping restores dystrophin expression in DMD patient derived muscle cells. , 2001, Human molecular genetics.

[15]  C. Samakovlis,et al.  A novel stop codon readthrough mechanism produces functional Headcase protein in Drosophila trachea , 2001, EMBO reports.

[16]  K. Fischbeck,et al.  Gentamicin treatment of Duchenne and Becker muscular dystrophy due to nonsense mutations , 2001, Annals of neurology.

[17]  J. Clancy,et al.  Evidence that systemic gentamicin suppresses premature stop mutations in patients with cystic fibrosis. , 2001, American journal of respiratory and critical care medicine.

[18]  R. Kapsa,et al.  In vivo and in vitro correction of the mdx dystrophin gene nonsense mutation by short-fragment homologous replacement. , 2001, Human gene therapy.

[19]  Peter E. Nielsen,et al.  Bactericidal antisense effects of peptide–PNA conjugates , 2001, Nature Biotechnology.

[20]  J. Thompson,et al.  Gentamicin-mediated suppression of Hurler syndrome stop mutations restores a low level of alpha-L-iduronidase activity and reduces lysosomal glycosaminoglycan accumulation. , 2001, Human molecular genetics.

[21]  I. Stansfield,et al.  Endless possibilities: translation termination and stop codon recognition. , 2001, Microbiology.

[22]  K. Flanigan,et al.  Sequence specificity of aminoglycoside‐induced stop codon readthrough: Potential implications for treatment of Duchenne muscular dystrophy , 2000, Annals of neurology.

[23]  D. Bedwell,et al.  Aminoglycoside antibiotics mediate context-dependent suppression of termination codons in a mammalian translation system. , 2000, RNA.

[24]  R. Schroeder,et al.  Modulation of RNA function by aminoglycoside antibiotics , 2000, The EMBO journal.

[25]  R. Kaufman,et al.  Correction of genetic disease by making sense from nonsense. , 1999, The Journal of clinical investigation.

[26]  J. Clancy,et al.  Suppression of a CFTR premature stop mutation in a bronchial epithelial cell line , 1997, Nature Medicine.

[27]  P. Nielsen,et al.  Progress in developing PNA as a gene-targeted drug. , 1997, Antisense & nucleic acid drug development.

[28]  T. Jilling,et al.  cAMP-regulated trafficking of epitope-tagged CFTR. , 1996, Kidney international.

[29]  M. Yarus,et al.  A simple and sensitive in vivo luciferase assay for tRNA-mediated nonsense suppression , 1990, Journal of bacteriology.

[30]  L. Nitschke,et al.  Aminoglycoside suppression at UAG, UAA and UGA codons inEscherichia coli and human tissue culture cells , 1989, Molecular and General Genetics MGG.

[31]  M. Yarus,et al.  Use of tRNA suppressors to probe regulation of Escherichia coli release factor 2. , 1988, Journal of molecular biology.

[32]  J. Wilhelm,et al.  Fidelity of the eukaryotic codon-anticodon interaction: interference by aminoglycoside antibiotics. , 1984, Biochemistry.

[33]  M. Sekiguchi,et al.  Mutants of Escherichia coli permeable to actinomycin. , 1967, Proceedings of the National Academy of Sciences of the United States of America.

[34]  A. Björnsson,et al.  The analysis of translational activity using a reporter gene constructed from repeats of an antibody-binding domain from protein A. , 1998, Methods in molecular biology.

[35]  V. McKusick Mendelian Inheritance in Man: A Catalog of Human Genes and Genetic Disorders , 1997 .

[36]  M Bobrow,et al.  Searching for the 1 in 2,400,000: A review of dystrophin gene point mutations , 1994, Human mutation.