Trinucleotide repeats affect DNA replication in vivo

[1]  S C Harvey,et al.  Flexible DNA: Genetically Unstable CTG·CAG and CGG·CCG from Human Hereditary Neuromuscular Disease Genes* , 1997, The Journal of Biological Chemistry.

[2]  R. Wells,et al.  Hairpin Formation during DNA Synthesis Primer Realignmentin Vitro in Triplet Repeat Sequences from Human Hereditary Disease Genes* , 1997, The Journal of Biological Chemistry.

[3]  Dmitry A. Gordenin,et al.  Repeat expansion — all in flap? , 1997, Nature Genetics.

[4]  S. Mirkin,et al.  Characteristic enrichment of DNA repeats in different genomes. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[5]  A. S. Krasilnikov,et al.  Mechanisms of triplex-caused polymerization arrest. , 1997, Nucleic acids research.

[6]  I. Haworth,et al.  At physiological pH, d(CCG)15 forms a hairpin containing protonated cytosines and a distorted helix. , 1997, Biochemistry.

[7]  R. Kolodner,et al.  A Novel Mutation Avoidance Mechanism Dependent on S. cerevisiae RAD27 Is Distinct from DNA Mismatch Repair , 1997, Cell.

[8]  M. Zheng,et al.  Genetically unstable CXG repeats are structurally dynamic and have a high propensity for folding. An NMR and UV spectroscopic study. , 1996, Journal of molecular biology.

[9]  R. Sinden,et al.  Relationship between Escherichia coli growth and deletions of CTG.CAG triplet repeats in plasmids. , 1996, Journal of molecular biology.

[10]  A. C. Chinault,et al.  Large domains of apparent delayed replication timing associated with triplet repeat expansion at FRAXA and FRAXE. , 1996, American journal of human genetics.

[11]  Myron F. Goodman,et al.  Gene Targeting in Rat Embryo Fibroblasts Promoted by the Polyomavirus Large T Antigen Associated With Neurological Diseases , 1996 .

[12]  R. Wells,et al.  CTG triplet repeats from the myotonic dystrophy gene are expanded in Escherichia coli distal to the replication origin as a single large event. , 1996, Journal of molecular biology.

[13]  R. Gellibolian,et al.  Cloning, characterization and properties of plasmids containing CGG triplet repeats from the FMR-1 gene. , 1996, Journal of molecular biology.

[14]  R. Wells.  Molecular Basis of Genetic Instability of Triplet Repeats (*) , 1996, The Journal of Biological Chemistry.

[15]  R. Wells,et al.  CTG Triplet Repeats from Human Hereditary Diseases Are Dominant Genetic Expansion Products in Escherichia coli(*) , 1996, The Journal of Biological Chemistry.

[16]  D. Patel,et al.  Solution structure of a DNA quadruplex containing the fragile X syndrome triplet repeat. , 1995, Journal of molecular biology.

[17]  R. Sinden,et al.  Mismatch repair in Escherichia coli enhances instability of (CTG)n triplet repeats from human hereditary diseases. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[18]  R. Wells,et al.  Pausing of DNA Synthesis in Vitro at Specific Loci in CTG and CGG Triplet Repeats from Human Hereditary Disease Genes (*) , 1995, The Journal of Biological Chemistry.

[19]  K. Woodford,et al.  CGG repeats associated with DNA instability and chromosome fragility form structures that block DNA synthesis in vitro. , 1995, Nucleic acids research.

[20]  I. Haworth,et al.  The trinucleotide repeat sequence d(GTC)15 adopts a hairpin conformation. , 1995, Nucleic acids research.

[21]  J. Mitchell,et al.  Compact structures of d(CNG)n oligonucleotides in solution and their possible relevance to fragile X and related human genetic diseases. , 1995, Nucleic acids research.

[22]  Keiichi Ohshima,et al.  Expansion and deletion of CTG repeats from human disease genes are determined by the direction of replication in E. coli , 1995, Nature Genetics.

[23]  S. S. Smith,et al.  Hairpins are formed by the single DNA strands of the fragile X triplet repeats: structure and biological implications. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[24]  A. Marquis Gacy,et al.  Trinucleotide repeats that expand in human disease form hairpin structures in vitro , 1995, Cell.

[25]  T. Jovin,et al.  Triad-DNA: a model for trinucleotide repeats , 1995, Nature Genetics.

[26]  B. J. Brewer,et al.  Analysis of replication intermediates by two-dimensional agarose gel electrophoresis. , 1995, Methods in enzymology.

[27]  S. Warren,et al.  Trinucleotide repeat expansion and human disease. , 1995, Annual review of genetics.

[28]  B. Alberts,et al.  The rapid dissociation of the T4 DNA polymerase holoenzyme when stopped by a DNA hairpin helix. A model for polymerase release following the termination of each Okazaki fragment. , 1994, The Journal of biological chemistry.

[29]  D. Schaid,et al.  Sequence analysis of the fragile X trinucleotide repeat: implications for the origin of the fragile X mutation. , 1994, Human molecular genetics.

[30]  J. Lebowitz,et al.  Transcription induces the formation of a stable RNA.DNA hybrid in the immunoglobulin alpha switch region. , 1994, The Journal of biological chemistry.

[31]  S. Warren,et al.  Cryptic and polar variation of the fragile X repeat could result in predisposing normal alleles , 1994, Cell.

[32]  A. Harding,et al.  Effect of trinucleotide repeat length and parental sex on phenotypic variation in spinocerebellar ataxia I. , 1994, American journal of human genetics.

[33]  L. Loeb,et al.  The fragile X syndrome d(CGG)n nucleotide repeats form a stable tetrahelical structure. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[34]  H. Lehrach,et al.  Trinucleotide repeat expansions and human genetic disease. , 1994, BioEssays : news and reviews in molecular, cellular and developmental biology.

[35]  A L Reiss,et al.  Frequency and stability of the fragile X premutation. , 1994, Human molecular genetics.

[36]  H. Wang,et al.  A single trinucleotide, 5'AGC3'/5'GCT3', of the triplet-repeat disease genes confers metal ion-induced non-B DNA structure. , 1993, Nucleic acids research.

[37]  S. Mirkin,et al.  Suicidal nucleotide sequences for DNA polymerization. , 1993, The EMBO journal.

[38]  Tomas A. Prolla,et al.  Destabilization of tracts of simple repetitive DNA in yeast by mutations affecting DNA mismatch repair , 1993, Nature.

[39]  T. Canfield,et al.  Association of fragile X syndrome with delayed replication of the FMR1 gene , 1993, Cell.

[40]  T. Webb.  Delayed replication of Xq27 in individuals with the fragile X syndrome. , 1992, American journal of medical genetics.

[41]  D. Lilley,et al.  DNA replication, 2nd edn , 1992 .

[42]  D. Nelson,et al.  Triplet repeat mutations in human disease. , 1992, Science.

[43]  J. Schvartzman,et al.  Unidirectional replication as visualized by two-dimensional agarose gel electrophoresis. , 1991, Journal of molecular biology.

[44]  R. Sinden,et al.  Preferential DNA secondary structure mutagenesis in the lagging strand of replication in E. coli , 1991, Nature.

[45]  J. Griffin,et al.  Induction of RNA-stabilized DMA conformers by transcription of an immunoglobulin switch region , 1990, Nature.

[46]  E. Amann,et al.  Tightly regulated tac promoter vectors useful for the expression of unfused and fused proteins in Escherichia coli. , 1988, Gene.

[47]  W. L. Fangman,et al.  The localization of replication origins on ARS plasmids in S. cerevisiae , 1987, Cell.

[48]  F. Bolivar,et al.  Plasmid vector pBR322 and its special-purpose derivatives--a review. , 1986, Gene.

[49]  D. Clewell,et al.  Nature of Col E1 Plasmid Replication in Escherichia coli in the Presence of Chloramphenicol , 1972, Journal of bacteriology.