Excess MCM proteins protect human cells from replicative stress by licensing backup origins of replication. - Wikidata - wikimedia - TriplyDB

Excess MCM proteins protect human cells from replicative stress by licensing backup origins of replication.

Excess MCM proteins protect human cells from replicative stress by licensing backup origins of replication.

http://www.wikidata.org/entity/Q36752433

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Interactions of the human MCM-BP protein with MCM complex components and Dbf4 Repriming of DNA synthesis at stalled replication forks by human PrimPol Initiation of DNA replication: functional and evolutionary aspects Replication licensing and cancer--a fatal entanglement?A double-hexameric MCM2-7 complex is loaded onto origin DNA during licensing of eukaryotic DNA replication Peaks cloaked in the mist: the landscape of mammalian replication origins Rescuing stalled or damaged replication forks The Mcm2-7 replicative helicase: a promising chemotherapeutic target A Role for USP7 in DNA Replication Differences in the DNA replication of unicellular eukaryotes and metazoans: known unknowns How MCM loading and spreading specify eukaryotic DNA replication initiation sites Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability Preventing replication fork collapse to maintain genome integrity Minichromosome maintenance helicase paralog MCM9 is dispensible for DNA replication but functions in germ-line stem cells and tumor suppression A reduction of licensed origins reveals strain-specific replication dynamics in mice USP7 is a SUMO deubiquitinase essential for DNA replication Accumulation of DNA damage in the aged hematopoietic stem cell compartment ATR checkpoint kinase and CRL1βTRCP collaborate to degrade ASF1a and thus repress genes overlapping with clusters of stalled replication forks.Cohesin organizes chromatin loops at DNA replication factories.Cdc45 limits replicon usage from a low density of preRCs in mammalian cells The role of the Fanconi anemia network in the response to DNA replication stress.ATR activation and replication fork restart are defective in FANCM-deficient cells.Human cytomegalovirus protein pUL117 targets the mini-chromosome maintenance complex and suppresses cellular DNA synthesis.Cytometry of chromatin bound Mcm6 and PCNA identifies two states in G1 that are separated functionally by the G1 restriction point.A concomitant loss of dormant origins and FANCC exacerbates genome instability by impairing DNA replication fork progression.Preferential re-replication of Drosophila heterochromatin in the absence of geminin.Incremental genetic perturbations to MCM2-7 expression and subcellular distribution reveal exquisite sensitivity of mice to DNA replication stress.The effects of oligomerization on Saccharomyces cerevisiae Mcm4/6/7 function Human Adipose-Derived Stem Cells Expanded Under Ambient Oxygen Concentration Accumulate Oxidative DNA Lesions and Experience Procarcinogenic DNA Replication Stress Phosphorylation of Mcm2 modulates Mcm2-7 activity and affects the cell's response to DNA damage DNA damage response and tumorigenesis in Mcm2-deficient mice Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription Decreased MCM2-6 in Drosophila S2 cells does not generate significant DNA damage or cause a marked increase in sensitivity to replication interference.MicroRNA-31 suppresses medulloblastoma cell growth by inhibiting DNA replication through minichromosome maintenance 2 The interaction between checkpoint kinase 1 (Chk1) and the minichromosome maintenance (MCM) complex is required for DNA damage-induced Chk1 phosphorylation.Chk1 promotes replication fork progression by controlling replication initiation.Evaluating genome-scale approaches to eukaryotic DNA replication.Chromatin replication and epigenome maintenance.BRG1 co-localizes with DNA replication factors and is required for efficient replication fork progression Increases in mitochondrial DNA content and 4977-bp deletion upon ATM/Chk2 checkpoint activation in HeLa cells.

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P2860

Excess MCM proteins protect human cells from replicative stress by licensing backup origins of replication.

http://www.wikidata.org/entity/Q36752433

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Excess MCM proteins protect hu ...... backup origins of replication.

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type

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Excess MCM proteins protect hu ...... backup origins of replication.

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Excess MCM proteins protect hu ...... backup origins of replication.

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Proceedings of the National Academy of Sciences of the United States of America

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Excess MCM proteins protect hu ...... backup origins of replication

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Arkaitz Ibarra

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P2860

Interaction between human MCM7 and Rad17 proteins is required for replication checkpoint signaling

Chromatin association of human origin recognition complex, cdc6, and minichromosome maintenance proteins during the cell cycle: assembly of prereplication complexes in late mitosis

Activation of mammalian Chk1 during DNA replication arrest: a role for Chk1 in the intra-S phase checkpoint monitoring replication origin firing

Isolation of the Cdc45/Mcm2-7/GINS (CMG) complex, a candidate for the eukaryotic DNA replication fork helicase

Minichromosome maintenance proteins are direct targets of the ATM and ATR checkpoint kinases

Replication protein A-mediated recruitment and activation of Rad17 complexes

Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

Replication foci dynamics: replication patterns are modulated by S-phase checkpoint kinases in fission yeast.

Inhibition of human Chk1 causes increased initiation of DNA replication, phosphorylation of ATR targets, and DNA breakage

ATR and ATM regulate the timing of DNA replication origin firing.

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