Pathological replication in cells lacking RecG DNA translocase.
about
Replication Termination: Containing Fork Fusion-Mediated Pathologies in Escherichia coliI came to a fork in the DNA and there was RecGThe C-terminal domain of the bacterial SSB protein acts as a DNA maintenance hub at active chromosome replication forksATP-dependent RecG helicase is required for the transcriptional regulator OxyR function in Pseudomonas speciesNovel Conserved Genotypes Correspond to Antibiotic Resistance Phenotypes of E. coli Clinical IsolatesOn the viability of Escherichia coli cells lacking DNA topoisomerase IReplication fork reversal after replication-transcription collision.Recombination and replication.Escherichia coli RecG functionally suppresses human Bloom syndrome phenotypesThe mtDNA mutation spectrum of the progeroid Polg mutator mouse includes abundant control region multimersBranch migration prevents DNA loss during double-strand break repairRECG maintains plastid and mitochondrial genome stability by suppressing extensive recombination between short dispersed repeatsDouble-Strand Break Repair and Holliday Junction Processing Are Required for Chromosome Processing in Stationary-Phase Escherichia coli CellsRecG Directs DNA Synthesis during Double-Strand Break Repair.Characterization of the Neisseria meningitidis Helicase RecG.Mycobacterium tuberculosis RecG binds and unwinds model DNA substrates with a preference for Holliday junctions.Superfamily 2 helicasesEffects of conserved residues and naturally occurring mutations on Mycobacterium tuberculosis RecG helicase activity.Recruitment to stalled replication forks of the PriA DNA helicase and replisome-loading activities is essential for survival.RecG controls DNA amplification at double-strand breaks and arrested replication forks.Replication Restart in Bacteria.25 years on and no end in sight: a perspective on the role of RecG proteinDifferent genome stability proteins underpin primed and naïve adaptation in E. coli CRISPR-Cas immunity.The Consequences of Replicating in the Wrong Orientation: Bacterial Chromosome Duplication without an Active Replication OriginPromoting and avoiding recombination: contrasting activities of the Escherichia coli RuvABC Holliday junction resolvase and RecG DNA translocase.Lambda gpP-DnaB Helicase Sequestration and gpP-RpoB Associated Effects: On Screens for Auxotrophs, Selection for Rif(R), Toxicity, Mutagenicity, Plasmid Curing.Modulation of DNA damage tolerance in Escherichia coli recG and ruv strains by mutations affecting PriB, the ribosome and RNA polymerase.RecG protein and single-strand DNA exonucleases avoid cell lethality associated with PriA helicase activity in Escherichia coli.Are the SSB-Interacting Proteins RecO, RecG, PriA and the DnaB-Interacting Protein Rep Bound to Progressing Replication Forks in Escherichia coli?Replication fork collisions cause pathological chromosomal amplification in cells lacking RecG DNA translocaseEvidence for the role of Mycobacterium tuberculosis RecG helicase in DNA repair and recombination.Mitochondrial helicase Irc3 translocates along double-stranded DNA.Chromosomal over-replication in Escherichia coli recG cells is triggered by replication fork fusion and amplified if replichore symmetry is disturbedReplication Fork Breakage and Restart in Escherichia coli
P2860
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P2860
Pathological replication in cells lacking RecG DNA translocase.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
2009年论文
@zh
2009年论文
@zh-cn
name
Pathological replication in cells lacking RecG DNA translocase.
@en
type
label
Pathological replication in cells lacking RecG DNA translocase.
@en
prefLabel
Pathological replication in cells lacking RecG DNA translocase.
@en
P2093
P2860
P1476
Pathological replication in cells lacking RecG DNA translocase.
@en
P2093
Amy L Upton
Christian J Rudolph
Lynda Harris
P2860
P304
P356
10.1111/J.1365-2958.2009.06773.X
P407
P577
2009-06-16T00:00:00Z