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