Cell cycle control of replication initiation in eukaryotes

Stephane Chevalier, J. Julian Blow

    Research output: Contribution to journalArticle

    43 Citations (Scopus)

    Abstract

    Studies on the initiation of DNA replication in eukaryotes have progressed recently through different approaches that promise to converge. Proteins interacting with the origin recognition complex form a prereplicative complex early in the cell cycle. The regulation of the binding of MCM/P1 proteins to chromatin plays a key role in the replication licensing system which prevents re-replication in a single cell cycle. Cyclin-dependent kinases provide an overall control of the cell cycle by stimulating S-phase entry and possibly by preventing re-establishment of prereplicative complexes in G2 phase.
    Original languageEnglish
    Pages (from-to)815-821
    Number of pages7
    JournalCurrent Opinion in Cell Biology
    Volume8
    Issue number6
    DOIs
    Publication statusPublished - Dec 1996

    Fingerprint

    Cell Cycle Checkpoints
    Eukaryota
    Cell Cycle
    Origin Recognition Complex
    Cyclin-Dependent Kinases
    G2 Phase
    Licensure
    DNA Replication
    S Phase
    Chromatin
    Proteins

    Cite this

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    Cell cycle control of replication initiation in eukaryotes. / Chevalier, Stephane; Blow, J. Julian.

    In: Current Opinion in Cell Biology, Vol. 8, No. 6, 12.1996, p. 815-821.

    Research output: Contribution to journalArticle

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    AU - Blow, J. Julian

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    AB - Studies on the initiation of DNA replication in eukaryotes have progressed recently through different approaches that promise to converge. Proteins interacting with the origin recognition complex form a prereplicative complex early in the cell cycle. The regulation of the binding of MCM/P1 proteins to chromatin plays a key role in the replication licensing system which prevents re-replication in a single cell cycle. Cyclin-dependent kinases provide an overall control of the cell cycle by stimulating S-phase entry and possibly by preventing re-establishment of prereplicative complexes in G2 phase.

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