Stimulation of flap endonuclease-1 by the Bloom's syndrome protein (Q24302463)

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Joshua A Sommers

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Leonard Wu

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Ian D Hickson

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Robert M Brosh

Journal of Biological Chemistry

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language of work or name

English

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publication date

12 March 2004

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published in

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volume

279

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issue

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page(s)

9847-56

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cites work

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Positional cloning of the Werner's syndrome gene

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Mutations in RECQL4 cause a subset of cases of Rothmund-Thomson syndrome

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The Bloom's syndrome gene product is a 3'-5' DNA helicase

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Binding and melting of D-loops by the Bloom syndrome helicase

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Oligomeric ring structure of the Bloom's syndrome helicase

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Characterization and mutational analysis of the RecQ core of the bloom syndrome protein

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BLM helicase-dependent transport of p53 to sites of stalled DNA replication forks modulates homologous recombination

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The processing of Holliday junctions by BLM and WRN helicases is regulated by p53

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Colocalization, physical, and functional interaction between Werner and Bloom syndrome proteins

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The Bloom's syndrome protein (BLM) interacts with MLH1 but is not required for DNA mismatch repair

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Direct association of Bloom's syndrome gene product with the human mismatch repair protein MLH1

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Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity

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

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Werner syndrome protein interacts with human flap endonuclease 1 and stimulates its cleavage activity

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The exonucleolytic and endonucleolytic cleavage activities of human exonuclease 1 are stimulated by an interaction with the carboxyl-terminal region of the Werner syndrome protein

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Haploinsufficiency of Flap endonuclease (Fen1) leads to rapid tumor progression

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Flap endonuclease 1: a novel tumour suppresser protein

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Multiple pathways cooperate in the suppression of genome instability in Saccharomyces cerevisiae

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Involvement of SGS1 in DNA damage-induced heteroallelic recombination that requires RAD52 in Saccharomyces cerevisiae

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Telomere-binding protein TRF2 binds to and stimulates the Werner and Bloom syndrome helicases

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The DNA helicase activity of BLM is necessary for the correction of the genomic instability of bloom syndrome cells

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The human Bloom syndrome gene suppresses the DNA replication and repair defects of yeast dna2 mutants

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The C-terminal domain of the Bloom syndrome DNA helicase is essential for genomic stability

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The Bloom's syndrome helicase suppresses crossing over during homologous recombination

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A yeast replicative helicase, Dna2 helicase, interacts with yeast FEN-1 nuclease in carrying out its essential function

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Rothmund-Thomson syndrome due to RECQ4 helicase mutations: report and clinical and molecular comparisons with Bloom syndrome and Werner syndrome

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7 January 2021

A novel mutation avoidance mechanism dependent on S. cerevisiae RAD27 is distinct from DNA mismatch repair

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7 January 2021

Elevation of sister chromatid exchange in Saccharomyces cerevisiae sgs1 disruptants and the relevance of the disruptants as a system to evaluate mutations in Bloom's syndrome gene

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7 January 2021

The Bloom's syndrome helicase unwinds G4 DNA

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7 January 2021

Unwinding of a DNA triple helix by the Werner and Bloom syndrome helicases

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7 January 2021

Biochemical characterization of the DNA substrate specificity of Werner syndrome helicase

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7 January 2021