Mismatch repair protein MutL becomes limiting during stationary-phase mutation. - Wikidata - awgldk - TriplyDB

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

http://www.wikidata.org/entity/Q35190848

about

Evidence that selected amplification of a bacterial lac frameshift allele stimulates Lac(+) reversion (adaptive mutation) with or without general hypermutability A phylogenomic study of the MutS family of proteins Barriers to genetic exchange between bacterial species: Streptococcus pneumoniae transformation Adaptive mutation: implications for evolution Adaptive amplification and point mutation are independent mechanisms: evidence for various stress-inducible mutation mechanisms Culture history and population heterogeneity as determinants of bacterial adaptation: the adaptomics of a single environmental transition Atypical Role for PhoU in Mutagenic Break Repair under Stress in Escherichia coli Mutational analysis of the MutH protein from Escherichia coli.On the mechanism of gene amplification induced under stress in Escherichia coli Are adaptive mutations due to a decline in mismatch repair? The evidence is lacking Identification of a regulator that controls stationary-phase expression of catalase-peroxidase in Caulobacter crescentus.Mechanisms of mutation in nondividing cells. Insights from the study of adaptive mutation in Escherichia coli.Engineering reduced evolutionary potential for synthetic biology Levels of the Vsr endonuclease do not regulate stationary-phase reversion of a Lac- frameshift allele in Escherichia coli.Hypermutation in bacteria and other cellular systems Multiprobe RNase protection assay analysis of mRNA levels for the Escherichia coli oxidative DNA glycosylase genes under conditions of oxidative stress.Role of the dinB gene product in spontaneous mutation in Escherichia coli with an impaired replicative polymerase.Mechanisms of stationary phase mutation: a decade of adaptive mutation Inactivation of the DNA repair genes mutS, mutL or the anti-recombination gene mutS2 leads to activation of vitamin B1 biosynthesis genes.The SOS response regulates adaptive mutation.Roles of FrxA and RdxA nitroreductases of Helicobacter pylori in susceptibility and resistance to metronidazole.Cooperation and competition in mismatch repair: very short-patch repair and methyl-directed mismatch repair in Escherichia coli.Regulation of mutY and nature of mutator mutations in Escherichia coli populations under nutrient limitation.DNA Mismatch Repair.Transient and heritable mutators in adaptive evolution in the lab and in nature.Adaptive mutation: has the unicorn landed?The chromosome bias of misincorporations during double-strand break repair is not altered in mismatch repair-defective strains of Saccharomyces cerevisiae.Increased episomal replication accounts for the high rate of adaptive mutation in recD mutants of Escherichia coli.Some features of the mutability of bacteria during nonlethal selection Evidence that stationary-phase hypermutation in the Escherichia coli chromosome is promoted by recombination.Saturation of DNA mismatch repair and error catastrophe by a base analogue in Escherichia coli.General stress response regulator RpoS in adaptive mutation and amplification in Escherichia coli.Adaptive mutation in Saccharomyces cerevisiae.Negative regulation of mutS and mutH repair gene expression by the Hfq and RpoS global regulators of Escherichia coli K-12.Complete and SOS-mediated response of Staphylococcus aureus to the antibiotic ciprofloxacin.Urinary tract infection drives genome instability in uropathogenic Escherichia coli and necessitates translesion synthesis DNA polymerase IV for virulence The frequency and structure of recombinant products is determined by the cellular level of MutL.Mutation as a stress response and the regulation of evolvability The role of transient hypermutators in adaptive mutation in Escherichia coli A shifting mutational landscape in 6 nutritional states: Stress-induced mutagenesis as a series of distinct stress input-mutation output relationships.

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P2860

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

http://www.wikidata.org/entity/Q35190848

description

1997 nî lūn-bûn

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1997 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

1997 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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1997年の論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年论文

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name

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

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Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

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type

label

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

@ast

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

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prefLabel

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

@ast

Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

@en

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Mismatch repair protein MutL becomes limiting during stationary-phase mutation.

@en

P2093

C Thulin

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

G Feng

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K J Ross

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M E Winkler

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R S Harris

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R Sidhu

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S K Szigety

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S Longerich

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S M Rosenberg

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P2860

Adaptive mutation: the uses of adversity

Biochemistry of homologous recombination in Escherichia coli

Biochemistry and genetics of eukaryotic mismatch repair

Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over

Escherichia coli mutS-encoded protein binds to mismatched DNA base pairs

Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

Construction and characterization of new cloning vehicles. II. A multipurpose cloning system

The distribution of the numbers of mutants in bacterial populations

Products of DNA mismatch repair genes mutS and mutL are required for transcription-coupled nucleotide-excision repair of the lactose operon in Escherichia coli

The extreme mutator effect of Escherichia coli mutD5 results from saturation of mismatch repair by excessive DNA replication errors

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10.1101/GAD.11.18.2426

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18

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11

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1997-09-01T00:00:00Z

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9308969

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316514

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