Absence of BLM leads to accumulation of chromosomal DNA breaks during both unperturbed and disrupted S phases
about
ATR suppresses endogenous DNA damage and allows completion of homologous recombination repairBLAP75, an essential component of Bloom's syndrome protein complexes that maintain genome integrityRMI1/NCE4, a suppressor of genome instability, encodes a member of the RecQ helicase/Topo III complexHpz1 modulates the G1-S transition in fission yeastATR: an essential regulator of genome integritySUMO modification regulates BLM and RAD51 interaction at damaged replication forks.ATR-p53 restricts homologous recombination in response to replicative stress but does not limit DNA interstrand crosslink repair in lung cancer cells.Replisome instability, fork collapse, and gross chromosomal rearrangements arise synergistically from Mec1 kinase and RecQ helicase mutations.RecQ helicases: guardian angels of the DNA replication fork.Rad17 plays a central role in establishment of the interaction between TopBP1 and the Rad9-Hus1-Rad1 complex at stalled replication forksMechanistically distinct roles for Sgs1p in checkpoint activation and replication fork maintenance.Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.Human TopBP1 ensures genome integrity during normal S phaseFanconi anemia proteins are required to prevent accumulation of replication-associated DNA double-strand breaksPhosphorylation of Xenopus Rad1 and Hus1 defines a readout for ATR activation that is independent of Claspin and the Rad9 carboxy terminusATM and ATR promote Mre11 dependent restart of collapsed replication forks and prevent accumulation of DNA breaksThe Mre11-Rad50-Nbs1 (MRN) complex has a specific role in the activation of Chk1 in response to stalled replication forksSite-specific phosphorylation of a checkpoint mediator protein controls its responses to different DNA structuresBLM SUMOylation regulates ssDNA accumulation at stalled replication forks.Top3α is required during the convergent migration step of double Holliday junction dissolution.DNA structure-induced recruitment and activation of the Fanconi anemia pathway protein FANCD2Temporal separation of replication and recombination requires the intra-S checkpoint.Bloom's syndrome helicase and Mus81 are required to induce transient double-strand DNA breaks in response to DNA replication stressMechanisms of RecQ helicases in pathways of DNA metabolism and maintenance of genomic stabilityFANCD2 regulates BLM complex functions independently of FANCI to promote replication fork recovery.Smc5/6-mediated regulation of replication progression contributes to chromosome assembly during mitosis in human cells.DNA damage response: three levels of DNA repair regulation.PCNA-Ub polyubiquitination inhibits cell proliferation and induces cell-cycle checkpoints.Transplantation of adipose-derived stem cells combined with collagen scaffolds restores ovarian function in a rat model of premature ovarian insufficiency.
P2860
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P2860
Absence of BLM leads to accumulation of chromosomal DNA breaks during both unperturbed and disrupted S phases
description
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name
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
@ast
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
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type
label
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
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Absence of BLM leads to accumu ...... rturbed and disrupted S phases
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prefLabel
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
@ast
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
@en
P2093
P2860
P356
P1476
Absence of BLM leads to accumu ...... rturbed and disrupted S phases
@en
P2093
Soo-Mi Kim
William G Dunphy
P2860
P304
P356
10.1083/JCB.200402095
P407
P577
2004-06-14T00:00:00Z