about
The 3'-->5' exonuclease of DNA polymerase delta can substitute for the 5' flap endonuclease Rad27/Fen1 in processing Okazaki fragments and preventing genome instabilityMutational heterogeneity in cancer and the search for new cancer-associated genesThe multiple biological roles of the 3'-->5' exonuclease of Saccharomyces cerevisiae DNA polymerase delta require switching between the polymerase and exonuclease domainsFunctional analysis of human FEN1 in Saccharomyces cerevisiae and its role in genome stabilityOkazaki fragment maturation in yeast. II. Cooperation between the polymerase and 3'-5'-exonuclease activities of Pol delta in the creation of a ligatable nickThe somatic genomic landscape of chromophobe renal cell carcinomaHypermutation in human cancer genomes: footprints and mechanismsWho Is Leading the Replication Fork, Pol ε or Pol δ?Cohesin Is limiting for the suppression of DNA damage-induced recombination between homologous chromosomesBase damage within single-strand DNA underlies in vivo hypermutability induced by a ubiquitous environmental agentHypermutability of damaged single-strand DNA formed at double-strand breaks and uncapped telomeres in yeast Saccharomyces cerevisiae.Genome-wide model for the normal eukaryotic DNA replication fork.Alkylation base damage is converted into repairable double-strand breaks and complex intermediates in G2 cells lacking AP endonuclease.A novel role in DNA metabolism for the binding of Fen1/Rad27 to PCNA and implications for genetic risk.The prevention of repeat-associated deletions in Saccharomyces cerevisiae by mismatch repair depends on size and origin of deletions.Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitnessThe flexible loop of human FEN1 endonuclease is required for flap cleavage during DNA replication and repair.Heterogeneous polymerase fidelity and mismatch repair bias genome variation and composition.Genetic factors affecting the impact of DNA polymerase delta proofreading activity on mutation avoidance in yeast.Break-induced replication is a source of mutation clusters underlying kataegisSuppression of allelic recombination and aneuploidy by cohesin is independent of Chk1 in Saccharomyces cerevisiae.Damage-induced localized hypermutability.Mutator phenotypes of yeast strains heterozygous for mutations in the MSH2 gene.Conservative repair of a chromosomal double-strand break by single-strand DNA through two steps of annealing.Clustered mutations in yeast and in human cancers can arise from damaged long single-strand DNA regions.An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancersThe Impact of Environmental and Endogenous Damage on Somatic Mutation Load in Human Skin FibroblastsAPOBEC-Induced Cancer Mutations Are Uniquely Enriched in Early-Replicating, Gene-Dense, and Active Chromatin RegionsClusters of Multiple Mutations: Incidence and Molecular MechanismsReplication slippage between distant short repeats in Saccharomyces cerevisiae depends on the direction of replication and the RAD50 and RAD52 genes.Altered replication and inverted repeats induce mismatch repair-independent recombination between highly diverged DNAs in yeast.Hypermutability of homonucleotide runs in mismatch repair and DNA polymerase proofreading yeast mutants.Apn1 and Apn2 endonucleases prevent accumulation of repair-associated DNA breaks in budding yeast as revealed by direct chromosomal analysis.Inverted DNA repeats: a source of eukaryotic genomic instabilityRAD53 is limiting in double-strand break repair and in protection against toxicity associated with ribonucleotide reductase inhibitionFlexibility of eukaryotic Okazaki fragment maturation through regulated strand displacement synthesisThe transition of closely opposed lesions to double-strand breaks during long-patch base excision repair is prevented by the coordinated action of DNA polymerase delta and Rad27/Fen1.Cadmium is a mutagen that acts by inhibiting mismatch repair.An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers.The sister chromatid cohesion pathway suppresses multiple chromosome gain and chromosome amplification.
P50
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P50
description
researcher
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wetenschapper
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հետազոտող
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
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Dmitry A. Gordenin
@sl
P106
P1153
7003896563
P31
P496
0000-0002-8399-1836