Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage. - Wikidata - wikimedia - TriplyDB

Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.

Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.

http://www.wikidata.org/entity/Q34097292

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PML nuclear bodies Optimal function of the DNA repair enzyme TDP1 requires its phosphorylation by ATM and/or DNA-PK Inhibition of Topoisomerase (DNA) I (TOP1): DNA Damage Repair and Anticancer Therapy Disease-causing missense mutations in human DNA helicase disorders An N-terminal acidic region of Sgs1 interacts with Rpa70 and recruits Rad53 kinase to stalled forks.HCLK2 is essential for the mammalian S-phase checkpoint and impacts on Chk1 stability Promyelocytic leukemia nuclear bodies behave as DNA damage sensors whose response to DNA double-strand breaks is regulated by NBS1 and the kinases ATM, Chk2, and ATR.Topoisomerase IIIalpha is required for normal proliferation and telomere stability in alternative lengthening of telomeres.H2AX is required for cell cycle arrest via the p53/p21 pathway SUMO modification regulates BLM and RAD51 interaction at damaged replication forks.A helical bundle in the N-terminal domain of the BLM helicase mediates dimer and potentially hexamer formation.ATR and ATM differently regulate WRN to prevent DSBs at stalled replication forks and promote replication fork recovery.Human RECQ1 is a DNA damage responsive protein required for genotoxic stress resistance and suppression of sister chromatid exchanges.The G-quadruplex ligand telomestatin impairs binding of topoisomerase IIIalpha to G-quadruplex-forming oligonucleotides and uncaps telomeres in ALT cells Induction of homologous recombination following in utero exposure to DNA-damaging agents.Regulation of BLM Nucleolar Localization Chk1-dependent constitutive phosphorylation of BLM helicase at serine 646 decreases after DNA damage.The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinone The complexity of phosphorylated H2AX foci formation and DNA repair assembly at DNA double-strand breaks.A Rad53 independent function of Rad9 becomes crucial for genome maintenance in the absence of the Recq helicase Sgs1 Homologous recombination and its regulation Cellular defects caused by hypomorphic variants of the Bloom syndrome helicase gene BLM.Bloom's syndrome helicase and Mus81 are required to induce transient double-strand DNA breaks in response to DNA replication stress Repair of topoisomerase I-mediated DNA damage.Iron chelators with topoisomerase-inhibitory activity and their anticancer applications.Phosphorylation-dependent interactions of BLM and 53BP1 are required for their anti-recombinogenic roles during homologous recombination.Collaborating functions of BLM and DNA topoisomerase I in regulating human rDNA transcription The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs.Rising from the RecQ-age: the role of human RecQ helicases in genome maintenance Recql5 plays an important role in DNA replication and cell survival after camptothecin treatment.The BLM dissolvasome in DNA replication and repair.Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.DNA damage response: three levels of DNA repair regulation.Molecular mechanism of double Holliday junction dissolution.The iron chelator Dp44mT inhibits the proliferation of cancer cells but fails to protect from doxorubicin-induced cardiotoxicity in spontaneously hypertensive rats.Bocavirus infection induces a DNA damage response that facilitates viral DNA replication and mediates cell death.The human WRN and BLM RecQ helicases differentially regulate cell proliferation and survival after chemotherapeutic DNA damage.GTPase-mediated regulation of the unfolded protein response in Caenorhabditis elegans is dependent on the AAA+ ATPase CDC-48.The Walker B motif in avian FANCM is required to limit sister chromatid exchanges but is dispensable for DNA crosslink repair.

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Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.

http://www.wikidata.org/entity/Q34097292

description

2005 nî lūn-bûn

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2005 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2005 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

@ast

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

@en

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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type

label

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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prefLabel

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

@ast

Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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Phosphorylation of BLM, dissoc ...... I-induced replication damage.

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MCB.25.20.8925-8937.2005

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Molecular and Cellular Biology

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Phosphorylation of BLM, dissoc ...... I-induced replication damage.

@en

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Angela M Fan

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Christopher F Doe

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Ian D Hickson

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Linghua Meng

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Phillip S North

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V Ashutosh Rao

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P2860

DNA T OPOISOMERASES : Structure, Function, and Mechanism

Cellular roles of dna topoisomerases: a molecular perspective

Association of the Bloom syndrome protein with topoisomerase IIIalpha in somatic and meiotic cells

Nuclear structure in normal and Bloom syndrome cells

MDC1 is a mediator of the mammalian DNA damage checkpoint

BLAP75, an essential component of Bloom's syndrome protein complexes that maintain genome integrity

PML colocalizes with and stabilizes the DNA damage response protein TopBP1

Replication-mediated DNA damage by camptothecin induces phosphorylation of RPA by DNA-dependent protein kinase and dissociates RPA:DNA-PK complexes

The Bloom's syndrome helicase stimulates the activity of human topoisomerase IIIalpha

The Bloom's syndrome gene product promotes branch migration of holliday junctions

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10.1128/MCB.25.20.8925-8937.2005

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phosphorylation

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1265790

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