Specific pathways prevent duplication-mediated genome rearrangements. - Wikidata - awgldk - TriplyDB

Specific pathways prevent duplication-mediated genome rearrangements.

Specific pathways prevent duplication-mediated genome rearrangements.

http://www.wikidata.org/entity/Q41927457

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Multiple cellular mechanisms prevent chromosomal rearrangements involving repetitive DNA The Mre11:Rad50 Structure Shows an ATP-Dependent Molecular Clamp in DNA Double-Strand Break Repair ATP driven structural changes of the bacterial Mre11:Rad50 catalytic head complex Structural basis for DNA recognition and nuclease processing by the Mre11 homologue SbcD in double-strand breaks repair Distinct SUMO ligases cooperate with Esc2 and Slx5 to suppress duplication-mediated genome rearrangements A reversible histone H3 acetylation cooperates with mismatch repair and replicative polymerases in maintaining genome stability Dominant mutations in S. cerevisiae PMS1 identify the Mlh1-Pms1 endonuclease active site and an exonuclease 1-independent mismatch repair pathway Mismatch repair protein hMSH2-hMSH6 recognizes mismatches and forms sliding clamps within a D-loop recombination intermediate DNA repair pathway selection caused by defects in TEL1, SAE2, and de novo telomere addition generates specific chromosomal rearrangement signatures.A proteome-wide analysis of kinase-substrate network in the DNA damage response.Reconstitution of Saccharomyces cerevisiae DNA polymerase ε-dependent mismatch repair with purified proteins.Fusion of nearby inverted repeats by a replication-based mechanism leads to formation of dicentric and acentric chromosomes that cause genome instability in budding yeast.Post-replication repair suppresses duplication-mediated genome instability Formation of complex and unstable chromosomal translocations in yeast The roles of the Saccharomyces cerevisiae RecQ helicase SGS1 in meiotic genome surveillance.SUMO-targeted ubiquitin ligase, Rad60, and Nse2 SUMO ligase suppress spontaneous Top1-mediated DNA damage and genome instability.Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae A genetic and structural study of genome rearrangements mediated by high copy repeat Ty1 elements Diploid-specific [corrected] genome stability genes of S. cerevisiae: genomic screen reveals haploidization as an escape from persisting DNA rearrangement stress Chromosome rearrangements and aneuploidy in yeast strains lacking both Tel1p and Mec1p reflect deficiencies in two different mechanisms.Rapid analysis of Saccharomyces cerevisiae genome rearrangements by multiplex ligation-dependent probe amplification.The role of replication bypass pathways in dicentric chromosome formation in budding yeast Recovery of arrested replication forks by homologous recombination is error-prone.CENP-B preserves genome integrity at replication forks paused by retrotransposon LTR.Bridge-induced chromosome translocation in yeast relies upon a Rad54/Rdh54-dependent, Pol32-independent pathway Mutator activity induced by microRNA-155 (miR-155) links inflammation and cancer.Genome-wide analyses of LINE-LINE-mediated nonallelic homologous recombination.Phosphorylation of Sae2 Mediates Forkhead-associated (FHA) Domain-specific Interaction and Regulates Its DNA Repair Function.A genomic screen revealing the importance of vesicular trafficking pathways in genome maintenance and protection against genotoxic stress in diploid Saccharomyces cerevisiae cells Differential genetic interactions between Sgs1, DNA-damage checkpoint components and DNA repair factors in the maintenance of chromosome stability.Yeast Assay Highlights the Intrinsic Genomic Instability of Human PML Intron 6 over Intron 3 and the Role of Replication Fork Proteins Activation of Saccharomyces cerevisiae Mlh1-Pms1 Endonuclease in a Reconstituted Mismatch Repair System.The genetics of microdeletion and microduplication syndromes: an update.Fork rotation and DNA precatenation are restricted during DNA replication to prevent chromosomal instability.A Checkpoint-Related Function of the MCM Replicative Helicase Is Required to Avert Accumulation of RNA:DNA Hybrids during S-phase and Ensuing DSBs during G2/M Visualization of eukaryotic DNA mismatch repair reveals distinct recognition and repair intermediates.STUbLs in chromatin and genome stability.Bioinformatic identification of genes suppressing genome instability A personal historical view of DNA mismatch repair with an emphasis on eukaryotic DNA mismatch repair.Gene copy-number variation in haploid and diploid strains of the yeast Saccharomyces cerevisiae

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P2860

Specific pathways prevent duplication-mediated genome rearrangements.

http://www.wikidata.org/entity/Q41927457

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Specific pathways prevent duplication-mediated genome rearrangements.

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Specific pathways prevent duplication-mediated genome rearrangements.

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Specific pathways prevent duplication-mediated genome rearrangements.

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Specific pathways prevent duplication-mediated genome rearrangements.

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Christopher D Putnam

http://www.w3.org/2001/XMLSchema#string

Richard D Kolodner

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Tikvah K Hayes

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P2860

Components of the Ku-dependent non-homologous end-joining pathway are involved in telomeric length maintenance and telomeric silencing.

Requirement for three novel protein complexes in the absence of the Sgs1 DNA helicase in Saccharomyces cerevisiae

A system of shuttle vectors and yeast host strains designed for efficient manipulation of DNA in Saccharomyces cerevisiae

Holliday junctions accumulate in replication mutants via a RecA homolog-independent mechanism.

Yeast Mph1 helicase dissociates Rad51-made D-loops: implications for crossover control in mitotic recombination.

Role of Saccharomyces cerevisiae Msh2 and Msh3 repair proteins in double-strand break-induced recombination.

Break-induced replication and telomerase-independent telomere maintenance require Pol32.

The Srs2 helicase prevents recombination by disrupting Rad51 nucleoprotein filaments.

SGS1, the Saccharomyces cerevisiae homologue of BLM and WRN, suppresses genome instability and homeologous recombination.

RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO.

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