ArticleThe Journal of biological chemistry2008
Cdt1 forms a complex with the minichromosome maintenance protein (MCM) and activates its helicase activity.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Overexpression of CDT1 inhibits cell cycle progression at S phase by interacting with the mini-chromosome maintenance complex and causes DNA damage.FEBS open bio · 2026Article
- Aurora-A Promotes Cell-Cycle Progression From Quiescence Through Primary Cilia Disassembly.Cancer science · 2025Article
- SETD3-mediated histidine methylation of MCM7 regulates DNA replication by facilitating chromatin loading of MCM.Science China. Life sciences · 2025Article
- Recent advances in understanding DNA replication: cell type-specific adaptation of the DNA replication program.F1000Research · 2018Review
- Potent DNA strand annealing activity associated with mouse Mcm2∼7 heterohexameric complex.Nucleic acids research · 2017Article
- Mechanisms and regulation of DNA replication initiation in eukaryotes.Critical reviews in biochemistry and molecular biology · 2017Review
- Characterization of conserved arginine residues on Cdt1 that affect licensing activity and interaction with Geminin or Mcm complex.Cell cycle (Georgetown, Tex.) · 2016Article
- DNA replication origin activation in space and time.Nature reviews. Molecular cell biology · 2015Review
- Geminin inhibits a late step in the formation of human pre-replicative complexes.The Journal of biological chemistry · 2014Article
- Helicase loading at chromosomal origins of replication.Cold Spring Harbor perspectives in biology · 2013Review
- Article
- Structural insights into the Cdt1-mediated MCM2-7 chromatin loading.Nucleic acids research · 2012Article
- Depletion of cellular pre-replication complex factors results in increased human cytomegalovirus DNA replication.PloS one · 2012Article
- Abundance of prereplicative complexes (Pre-RCs) facilitates recombinational repair under replication stress in fission yeast.The Journal of biological chemistry · 2011Article
- Multiple Cdt1 molecules act at each origin to load replication-competent Mcm2-7 helicases.The EMBO journal · 2011Article
- Mass spectrometric studies on epigenetic interaction networks in cell differentiation.The Journal of biological chemistry · 2011Article
- Prevention of DNA re-replication in eukaryotic cells.Journal of molecular cell biology · 2011Review
- The effects of oligomerization on Saccharomyces cerevisiae Mcm4/6/7 function.BMC biochemistry · 2010Article
- Structure and mutagenesis studies of the C-terminal region of licensing factor Cdt1 enable the identification of key residues for binding to replicative helicase Mcm proteins.The Journal of biological chemistry · 2010Article
- Characterization and structure determination of the Cdt1 binding domain of human minichromosome maintenance (Mcm) 6.The Journal of biological chemistry · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mcm4/6/7 forms a complex possessing DNA helicase activity, suggesting that Mcm may be a central component for the replicative helicase. Although Cdt1 is known to be essential for loading of Mcm onto the chromatin, its precise role in pre-RC formation and replication initiation is unknown. Using purified proteins, we show that Cdt1 forms a complex with Mcm4/6/7, Mcm2/3/4/5/6/7, and Mcm2/4/6/7 in glycerol gradient fractionation through interaction with Mcm2 and Mcm4/6. In the glycerol gradient fractionation, Mcm4/6/7-Cdt1 forms a complex (speculated to be a (Mcm4/6/7)2-Cdt13 assembly) in the presence of ATP, which is significantly larger than the Mcm4/6/7-Cdt1 complex generated in its absence. Furthermore, DNA binding and helicase activities of Mcm4/6/7 are significantly stimulated by Cdt1 protein in vitro. We generated a Cdt1 mutant, which fails to stimulate DNA binding and helicase activities of Mcm4/6/7. This mutant Cdt1 showed reduced interaction with Mcm and is deficient in the formation of a high molecular weight complex with Mcm. Thus, a productive interaction between Cdt1 and MCM appears to be essential for efficient loading of MCM onto template DNA, as well as for the efficient unwinding reaction.
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