Nucleotide excision repair or polymerase V-mediated lesion bypass can act to restore UV-arrested replication forks in Escherichia coli.
about
Rescuing stalled or damaged replication forksTranslesion DNA synthesis and mutagenesis in prokaryotes.Recombination and replication.Translesion DNA Synthesis.Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli.Mfd is required for rapid recovery of transcription following UV-induced DNA damage but not oxidative DNA damage in Escherichia coli.Inactivation of the DnaB helicase leads to the collapse and degradation of the replication fork: a comparison to UV-induced arrest.Inefficient replication reduces RecA-mediated repair of UV-damaged plasmids introduced into competent Escherichia coliCellular characterization of the primosome and rep helicase in processing and restoration of replication following arrest by UV-induced DNA damage in Escherichia coli.Translesion DNA polymerases remodel the replisome and alter the speed of the replicative helicase.Shifting replication between IInd, IIIrd, and IVth gears.Nucleotide excision repair is a predominant mechanism for processing nitrofurazone-induced DNA damage in Escherichia coliGenetic analysis of repair and damage tolerance mechanisms for DNA-protein cross-links in Escherichia coli.Replication fork reversal and the maintenance of genome stabilityMultiple strategies for translesion synthesis in bacteriaA proposal: Source of single strand DNA that elicits the SOS response.Homologous recombination as a replication fork escort: fork-protection and recovery.The inactivation of rfaP, rarA or sspA gene improves the viability of the Escherichia coli DNA polymerase III holD mutant.25 years on and no end in sight: a perspective on the role of RecG proteinProcessing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.Replication fork stalling and cell cycle arrest in UV-irradiated Escherichia coli.Escherichia coli Fpg glycosylase is nonrendundant and required for the rapid global repair of oxidized purine and pyrimidine damage in vivoA ΔdinB mutation that sensitizes Escherichia coli to the lethal effects of UV- and X-radiation.Simulating the temporal modulation of inducible DNA damage response in Escherichia coli.RuvABC is required to resolve holliday junctions that accumulate following replication on damaged templates in Escherichia coli.
P2860
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P2860
Nucleotide excision repair or polymerase V-mediated lesion bypass can act to restore UV-arrested replication forks in Escherichia coli.
description
2005 nî lūn-bûn
@nan
2005 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@ast
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@en
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@nl
type
label
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@ast
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@en
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@nl
prefLabel
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@ast
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@en
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@nl
P2093
P2860
P1476
Nucleotide excision repair or ...... ion forks in Escherichia coli.
@en
P2093
Charmain T Courcelle
Jerilyn J Belle
Justin Courcelle
P2860
P304
P356
10.1128/JB.187.20.6953-6961.2005
P407
P577
2005-10-01T00:00:00Z