Enhanced genomic instability and defective postreplication repair in RAD18 knockout mouse embryonic stem cells
about
Effect of DNA repair protein Rad18 on viral infectionRAD18-BRCTx interaction is required for efficient repair of UV-induced DNA damageProliferating cell nuclear antigen (PCNA)-binding protein C1orf124 is a regulator of translesion synthesisBRCTx is a novel, highly conserved RAD18-interacting proteinPolyubiquitinated PCNA recruits the ZRANB3 translocase to maintain genomic integrity after replication stressRad18 guides poleta to replication stalling sites through physical interaction and PCNA monoubiquitinationHuman SHPRH suppresses genomic instability through proliferating cell nuclear antigen polyubiquitinationVertebrate DNA damage tolerance requires the C-terminus but not BRCT or transferase domains of REV1Coordination of DNA damage tolerance mechanisms with cell cycle progression in fission yeast.Human RAD18 interacts with ubiquitylated chromatin components and facilitates RAD9 recruitment to DNA double strand breaksExpression profiles of urbilaterian genes uniquely shared between honey bee and vertebratesZscan4 regulates telomere elongation and genomic stability in ES cellsDNA damage-specific deubiquitination regulates Rad18 functions to suppress mutagenesisRegulated expression and dynamic changes in subnuclear localization of mammalian Rad18 under normal and genotoxic conditionsCharacterization of human Spartan/C1orf124, an ubiquitin-PCNA interacting regulator of DNA damage toleranceDifferential regulation of Rad18 through Rad6-dependent mono- and polyubiquitinationLysine 63-polyubiquitination guards against translesion synthesis-induced mutations.Replication-dependent and -independent responses of RAD18 to DNA damage in human cells.Network architecture of signaling from uncoupled helicase-polymerase to cell cycle checkpoints and trans-lesion DNA synthesis.High mobility of flap endonuclease 1 and DNA polymerase eta associated with replication foci in mammalian S-phase nucleus.RAD18-dependent recruitment of SNM1A to DNA repair complexes by a ubiquitin-binding zinc finger.PCNA ubiquitination is important, but not essential for translesion DNA synthesis in mammalian cells.DNA template strand sequencing of single-cells maps genomic rearrangements at high resolution.RAD18-mediated ubiquitination of PCNA activates the Fanconi anemia DNA repair network.Role of the ubiquitin-binding domain of Polη in Rad18-independent translesion DNA synthesis in human cell extracts.Regulation of gross chromosomal rearrangements by ubiquitin and SUMO ligases in Saccharomyces cerevisiae.Phosphorylated Rad18 directs DNA polymerase η to sites of stalled replicationTwo replication fork maintenance pathways fuse inverted repeats to rearrange chromosomesDefining a genotoxic profile with mouse embryonic stem cellsMutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae.Kinetics of drug selection systems in mouse embryonic stem cellsSingle cell analysis of human RAD18-dependent DNA post-replication repair by alkaline bromodeoxyuridine comet assay.Tumour suppressor ING1b maintains genomic stability upon replication stress.RAD18 activates the G2/M checkpoint through DNA damage signaling to maintain genome integrity after ionizing radiation exposure.Meiotic functions of RAD18.Human RAD18 is involved in S phase-specific single-strand break repair without PCNA monoubiquitinationRAD18 and poly(ADP-ribose) polymerase independently suppress the access of nonhomologous end joining to double-strand breaks and facilitate homologous recombination-mediated repair.Functional characterization of Rad18 domains for Rad6, ubiquitin, DNA binding and PCNA modification.Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo.RAD18 and associated proteins are immobilized in nuclear foci in human cells entering S-phase with ultraviolet light-induced damage
P2860
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P2860
Enhanced genomic instability and defective postreplication repair in RAD18 knockout mouse embryonic stem cells
description
2003 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի հունվարին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2003
@ast
im Januar 2003 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2003/01/01)
@sk
vědecký článek publikovaný v roce 2003
@cs
wetenschappelijk artikel (gepubliceerd op 2003/01/01)
@nl
наукова стаття, опублікована в січні 2003
@uk
مقالة علمية (نشرت عام 2003)
@ar
name
Enhanced genomic instability a ...... out mouse embryonic stem cells
@ast
Enhanced genomic instability a ...... out mouse embryonic stem cells
@en
Enhanced genomic instability a ...... out mouse embryonic stem cells
@nl
type
label
Enhanced genomic instability a ...... out mouse embryonic stem cells
@ast
Enhanced genomic instability a ...... out mouse embryonic stem cells
@en
Enhanced genomic instability a ...... out mouse embryonic stem cells
@nl
prefLabel
Enhanced genomic instability a ...... out mouse embryonic stem cells
@ast
Enhanced genomic instability a ...... out mouse embryonic stem cells
@en
Enhanced genomic instability a ...... out mouse embryonic stem cells
@nl
P2093
P2860
P921
P3181
P1476
Enhanced genomic instability a ...... out mouse embryonic stem cells
@en
P2093
Hirokazu Inoue
Hitoshi Niwa
Masaru Yamaizumi
Satoshi Tateishi
Shiho Fujimoto
P2860
P304
P3181
P356
10.1128/MCB.23.2.474-481.2003
P407
P577
2003-01-01T00:00:00Z