Triplex-directed modification of genes and gene activity.

Oligonucleotides offer enormous potential for manipulating gene function in cells and, as such, constitute a promising new class of pharmaceutical agents. Oligonucleotides that form triple helices (triplexes) at specific DNA sequences in defined genes can be used to reduce transcription selectively, to introduce site-specific mutations or to stimulate gene-specific targeted recombination.

[1]  H. Krutzsch,et al.  Cellular Nucleic Acid Binding Protein Regulates the CT Element of the Human c- myc Protooncogene (*) , 1995, The Journal of Biological Chemistry.

[2]  M. Capecchi,et al.  Altering the genome by homologous recombination. , 1989, Science.

[3]  P. Glazer,et al.  Recombination induced by triple-helix-targeted DNA damage in mammalian cells , 1996, Molecular and cellular biology.

[4]  V. Vlassov,et al.  c-fos protooncogene transcription can be modulated by oligonucleotide-mediated formation of triplex structures in vitro. , 1996, European journal of biochemistry.

[5]  P. Glazer,et al.  Triplex DNA: fundamentals, advances, and potential applications for gene therapy , 1997, Journal of Molecular Medicine.

[6]  G. Hortobagyi,et al.  Recent advances in the application of gene therapy to human disease. , 1995, The American journal of medicine.

[7]  S. Mirkin,et al.  Triplex DNA structures. , 1995, Annual review of biochemistry.

[8]  C. Malvy,et al.  Investigation of the intracellular stability and formation of a triple helix formed with a short purine oligonucleotide targeted to the murine c-pim-1 proto-oncogene promotor. , 1996, Nucleic acids research.

[9]  M. Alunni-Fabbroni,et al.  Pyrimidine phosphorothioate oligonucleotides form triple-stranded helices and promote transcription inhibition. , 1994, Nucleic acids research.

[10]  A. Harel-Bellan,et al.  Detection of covalent triplex within human cells. , 1996, Nucleic acids research.

[11]  B. Wold,et al.  Analysis of promoter-specific repression by triple-helical DNA complexes in a eukaryotic cell-free transcription system. , 1992, Biochemistry.

[12]  Alexander Rich,et al.  FORMATION OF A THREE-STRANDED POLYNUCLEOTIDE MOLECULE , 1957 .

[13]  B. Lebleu,et al.  Reversible inhibition of gene expression by a psoralen functionalized triple helix forming oligonucleotide in intact cells. , 1994, The Journal of biological chemistry.

[14]  P. Dervan,et al.  Sequence-specific cleavage of double helical DNA by triple helix formation. , 1987, Science.

[15]  B. O’Malley,et al.  In vivo transcription of a progesterone-responsive gene is specifically inhibited by a triplex-forming oligonucleotide. , 1993, Nucleic acids research.

[16]  B. Aggarwal,et al.  Triple helix-forming oligodeoxyribonucleotides targeted to the human tumor necrosis factor (TNF) gene inhibit TNF production and block the TNF-dependent growth of human glioblastoma tumor cells. , 1996, Cancer research.

[17]  C. Malvy,et al.  Investigation of the formation and intracellular stability of purine.(purine/pyrimidine) triplexes. , 1997, Nucleic acids research.

[18]  K. Weber,et al.  Triple Helix-forming Oligonucleotide Corresponding to the Polypyrimidine Sequence in the Rat 1(I) Collagen Promoter Specifically Inhibits Factor Binding and Transcription (*) , 1996, The Journal of Biological Chemistry.

[19]  A. Bredberg,et al.  Triple helix directed psoralen adducts induce a low frequency of recombination in an SV40 shuttle vector. , 1995, Biochimica et biophysica acta.

[20]  M. Behe An overabundance of long oligopurine tracts occurs in the genome of simple and complex eukaryotes. , 1995, Nucleic acids research.

[21]  L. Israël,et al.  Temporary ex vivo inhibition of the expression of the human oncogene HER2 (NEU) by a triple helix-forming oligonucleotide. , 1996, Cancer research.

[22]  P. Glazer,et al.  Mutagenesis in Mammalian Cells Induced by Triple Helix Formation and Transcription-Coupled Repair , 1996, Science.

[23]  P. Glazer,et al.  Altered Repair of Targeted Psoralen Photoadducts in the Context of an Oligonucleotide-mediated Triple Helix (*) , 1995, The Journal of Biological Chemistry.

[24]  M. F. Shannon,et al.  DNA Triplex Formation Selectively Inhibits Granulocyte-Macrophage Colony-stimulating Factor Gene Expression in Human T Cells* , 1996, The Journal of Biological Chemistry.

[25]  C. Tu,et al.  Pentobarbital-induced Changes in Drosophila Glutathione S-Transferase D21 mRNA Stability (*) , 1995, The Journal of Biological Chemistry.

[26]  P. Glazer,et al.  Targeted mutagenesis in mammalian cells mediated by intracellular triple helix formation , 1995, Molecular and cellular biology.

[27]  K. Yamaguchi,et al.  Triplex-forming oligonucleotide binding represses transcription of the human c-erbB gene in glioma. , 1994, Growth factors.

[28]  Y. Israel,et al.  Inhibition of Gene Expression by Triple Helix Formation in Hepatoma Cells (*) , 1995, The Journal of Biological Chemistry.

[29]  D. Thomas,et al.  Oligonucleotide inhibition of IL2R alpha mRNA transcription by promoter region collinear triplex formation in lymphocytes. , 1991, Nucleic acids research.

[30]  P. Dervan,et al.  Second structural motif for recognition of DNA by oligonucleotide-directed triple-helix formation. , 1991, Science.

[31]  M. Hogan,et al.  High-affinity triple helix formation by synthetic oligonucleotides at a site within a selectable mammalian gene. , 1995, Biochemistry.

[32]  R. Wells,et al.  Specificity of the three-stranded complex formation between double-stranded DNA and single-stranded RNA containing repeating nucleotide sequences. , 1968, Journal of molecular biology.

[33]  M. Hogan,et al.  High-efficiency triple-helix-mediated photo-cross-linking at a targeted site within a selectable mammalian gene. , 1996, Biochemistry.

[34]  J. E. Gee,et al.  Triplex formation inhibits HER-2/neu transcription in vitro. , 1993, The Journal of clinical investigation.

[35]  S. Chandler,et al.  Specificity of antiparallel DNA triple helix formation. , 1996, Biochemistry.

[36]  D. Praseuth,et al.  Unexpected effect of an anti-human immunodeficiency virus intermolecular triplex-forming oligonucleotide in an in vitro transcription system due to RNase H-induced cleavage of the RNA transcript. , 1993, Antisense research and development.

[37]  M. Brenneman,et al.  Repair of site-specific double-strand breaks in a mammalian chromosome by homologous and illegitimate recombination , 1997, Molecular and cellular biology.

[38]  R. Rossen,et al.  Inhibition of transcription of HIV-1 in infected human cells by oligodeoxynucleotides designed to form DNA triple helices. , 1992, The Journal of biological chemistry.

[39]  M. Baccarani,et al.  Effect of unmodified triple helix‐forming oligodeoxyribonucleotide targeted to human multidrug‐resistance gene mdr1 in MDR cancer cells , 1994, FEBS letters.

[40]  T. Thomas,et al.  Suppression of c-myc oncogene expression by a polyamine-complexed triplex forming oligonucleotide in MCF-7 breast cancer cells. , 1995, Nucleic acids research.

[41]  S. J. Flint,et al.  Site-specific oligonucleotide binding represses transcription of the human c-myc gene in vitro. , 1988, Science.

[42]  D. Patel,et al.  DNA triplexes: solution structures, hydration sites, energetics, interactions, and function. , 1994, Biochemistry.