Structural basis for FEN-1 substrate specificity and PCNA-mediated activation in DNA replication and repair (Q27642925)

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David J Hosfield

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Seungil Han

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Junzhuan Qiu

4

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Biana Yelent

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Binghui Shen

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John A Tainer

Modeling of Flap Endonuclease Interactions with DNA Substrate

7

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language of work or name

English

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publication date

9 January 2004

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published in

Cell

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volume

116

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page(s)

39-50

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issue

1

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cites work

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A helical arch allowing single-stranded DNA to thread through T5 5'-exonuclease

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Interactions of mutant and wild-type flap endonucleases with oligonucleotide substrates suggest an alternative model of DNA binding

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Mutations in yeast proliferating cell nuclear antigen define distinct sites for interaction with DNA polymerase delta and DNA polymerase epsilon

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Stimulation of eukaryotic flap endonuclease-1 activities by proliferating cell nuclear antigen (PCNA) is independent of its in vitro interaction via a consensus PCNA binding region

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The acetylatable lysines of human Fen1 are important for endo- and exonuclease activities

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Two modes of FEN1 binding to PCNA regulated by DNA.

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Structure of the C-terminal region of p21(WAF1/CIP1) complexed with human PCNA

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Functional domains within FEN-1 and RAD2 define a family of structure-specific endonucleases: implications for nucleotide excision repair

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Flap endonuclease 1: a novel tumour suppresser protein

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Newly discovered archaebacterial flap endonucleases show a structure-specific mechanism for DNA substrate binding and catalysis resembling human flap endonuclease-1.

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Structure of the DNA repair and replication endonuclease and exonuclease FEN-1: coupling DNA and PCNA binding to FEN-1 activity

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The crystal structure of flap endonuclease-1 from Methanococcus jannaschii

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Regulation of DNA replication and repair proteins through interaction with the front side of proliferating cell nuclear antigen

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Cleavage specificity of Saccharomyces cerevisiae flap endonuclease 1 suggests a double-flap structure as the cellular substrate

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Human flap endonuclease-1: conformational change upon binding to the flap DNA substrate and location of the Mg2+ binding site

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

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PCNA binding through a conserved motif

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