Base Pair Mismatch

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  Subject Areas on Research

  • A defined human system that supports bidirectional mismatch-provoked excision. 
  • A new assay to quantify in vivo repair of G:T mispairs by base excision repair. 
  • ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background. 
  • Alleles of the yeast Pms1 mismatch-repair gene that differentially affect recombination- and replication-related processes. 
  • Analysis of the excision step in human DNA mismatch repair. 
  • Analysis of the proteins involved in the in vivo repair of base-base mismatches and four-base loops formed during meiotic recombination in the yeast Saccharomyces cerevisiae. 
  • Antitumor activity of temozolomide combined with irinotecan is partly independent of O6-methylguanine-DNA methyltransferase and mismatch repair phenotypes in xenograft models. 
  • Association between IHC and MSI testing to identify mismatch repair-deficient patients with ovarian cancer. 
  • Base composition of mononucleotide runs affects DNA polymerase slippage and removal of frameshift intermediates by mismatch repair in Saccharomyces cerevisiae. 
  • Biochemical correlates of temozolomide sensitivity in pediatric solid tumor xenograft models. 
  • Caenorhabditis elegans DNA mismatch repair gene msh-2 is required for microsatellite stability and maintenance of genome integrity. 
  • Conversion of diploidy to haploidy. 
  • DNA mismatch repair and genetic instability. 
  • DNA mismatch repair: functions and mechanisms. 
  • DNA repair: a double-edged sword. 
  • DNA-dependent activation of the hMutSalpha ATPase. 
  • DNMT3b polymorphism and hereditary nonpolyposis colorectal cancer age of onset. 
  • Defining regional infusion treatment strategies for extremity melanoma: comparative analysis of melphalan and temozolomide as regional chemotherapeutic agents. 
  • Differential and simultaneous adenosine di- and triphosphate binding by MutS. 
  • Differential specificities and simultaneous occupancy of human MutSalpha nucleotide binding sites. 
  • Direct NMR Evidence that Transient Tautomeric and Anionic States in dG·dT Form Watson-Crick-like Base Pairs. 
  • Direct visualization of asymmetric adenine-nucleotide-induced conformational changes in MutL alpha. 
  • Discrete in vivo roles for the MutL homologs Mlh2p and Mlh3p in the removal of frameshift intermediates in budding yeast. 
  • Distinct MutS DNA-binding modes that are differentially modulated by ATP binding and hydrolysis. 
  • Dynamic basis for dG•dT misincorporation via tautomerization and ionization. 
  • Endonucleolytic function of MutLalpha in human mismatch repair. 
  • Environmental Effects on Guanine-Thymine Mispair Tautomerization Explored with Quantum Mechanical/Molecular Mechanical Free Energy Simulations. 
  • Faster algorithms for optimal multiple sequence alignment based on pairwise comparisons. 
  • Frameshift mutagenesis: the roles of primer-template misalignment and the nonhomologous end-joining pathway in Saccharomyces cerevisiae. 
  • Hereditary nonpolyposis colorectal cancer: preventive management. 
  • High rate of CAD gene amplification in human cells deficient in MLH1 or MSH6. 
  • High-throughput genotyping with single nucleotide polymorphisms. 
  • Human exonuclease I is required for 5' and 3' mismatch repair. 
  • Human mismatch repair: reconstitution of a nick-directed bidirectional reaction. 
  • In vivo requirement for RecJ, ExoVII, ExoI, and ExoX in methyl-directed mismatch repair. 
  • Involvement of the beta clamp in methyl-directed mismatch repair in vitro. 
  • Isolation and characterization of point mutations in mismatch repair genes that destabilize microsatellites in yeast. 
  • Mechanism of 5'-directed excision in human mismatch repair. 
  • Mechanisms in eukaryotic mismatch repair. 
  • Meiotic recombination involving heterozygous large insertions in Saccharomyces cerevisiae: formation and repair of large, unpaired DNA loops. 
  • Methyl-directed repair of DNA base-pair mismatches in vitro. 1983. 
  • Mismatch recognition and subsequent processing have distinct effects on mitotic recombination intermediates and outcomes in yeast. 
  • Mismatch repair deficiency does not mediate clinical resistance to temozolomide in malignant glioma. 
  • Mismatch repair-dependent iterative excision at irreparable O6-methylguanine lesions in human nuclear extracts. 
  • Modulation of MutS ATP hydrolysis by DNA cofactors. 
  • MutL traps MutS at a DNA mismatch. 
  • MutLalpha and proliferating cell nuclear antigen share binding sites on MutSbeta. 
  • Novel PMS1 alleles preferentially affect the repair of primer strand loops during DNA replication. 
  • Nucleotide-promoted release of hMutSalpha from heteroduplex DNA is consistent with an ATP-dependent translocation mechanism. 
  • PARP-1 enhances the mismatch-dependence of 5'-directed excision in human mismatch repair in vitro. 
  • Phenotypic analysis of hMSH2 mutations in mouse cells carrying human chromosomes. 
  • Poly(ADP-ribose) polymerase-1 inhibition reverses temozolomide resistance in a DNA mismatch repair-deficient malignant glioma xenograft. 
  • Probing conformational transitions towards mutagenic Watson-Crick-like G·T mismatches using off-resonance sugar carbon R1ρ relaxation dispersion. 
  • Reduced expression of hMSH2 and hMLH1 and risk of prostate cancer: a case-control study. 
  • Redundant exonuclease involvement in Escherichia coli methyl-directed mismatch repair. 
  • Regulation of mitotic homeologous recombination in yeast. Functions of mismatch repair and nucleotide excision repair genes. 
  • Removal of frameshift intermediates by mismatch repair proteins in Saccharomyces cerevisiae. 
  • Repair of large insertion/deletion heterologies in human nuclear extracts is directed by a 5' single-strand break and is independent of the mismatch repair system. 
  • Role of mismatch repair in the fidelity of RAD51- and RAD59-dependent recombination in Saccharomyces cerevisiae. 
  • Sequence composition and context effects on the generation and repair of frameshift intermediates in mononucleotide runs in Saccharomyces cerevisiae. 
  • Somatic mutation of hPMS2 as a possible cause of sporadic human colon cancer with microsatellite instability. 
  • Spontaneous frameshift mutations in Saccharomyces cerevisiae: accumulation during DNA replication and removal by proofreading and mismatch repair activities. 
  • Structural evidence for the rare tautomer hypothesis of spontaneous mutagenesis. 
  • Structure of the human MutSalpha DNA lesion recognition complex. 
  • Structures of mismatch replication errors observed in a DNA polymerase. 
  • Tagging single nucleotide polymorphisms in MBD4 are associated with risk of lung cancer in a Chinese population. 
  • The C-terminal domain of the adenine-DNA glycosylase MutY confers specificity for 8-oxoguanine.adenine mispairs and may have evolved from MutT, an 8-oxo-dGTPase. 
  • The MutL ATPase is required for mismatch repair. 
  • The N2-ethylguanine and the O6-ethyl- and O6-methylguanine lesions in DNA: contrasting responses from the "bypass" DNA polymerase eta and the replicative DNA polymerase alpha. 
  • The mismatch DNA repair heterodimer, hMSH2/6, regulates BLM helicase. 
  • The yeast HSM3 gene is not involved in DNA mismatch repair in rapidly dividing cells. 
  • Variation in efficiency of DNA mismatch repair at different sites in the yeast genome. 
  • hMutSalpha- and hMutLalpha-dependent phosphorylation of p53 in response to DNA methylator damage. 
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  Keywords of People

  • McLendon, Roger Edwin, Professor of Pathology, Pathology
  • Yan, Hai, Adjunct Professor of Pathology, Pathology