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Georgia Xouri et al.
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Mouse pre-replicative complex proteins colocalise and interact with the centrosome
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Depletion of licensing inhibitor geminin causes centrosome overduplication and mitotic defects
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Cyclin-dependent kinases phosphorylate human Cdt1 and induce its degradation
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Rereplication by depletion of geminin is seen regardless of p53 status and activates a G2/M checkpoint
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A dimerized coiled-coil domain and an adjoining part of geminin interact with two sites on Cdt1 for replication inhibition
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Geminin has dimerization, Cdt1-binding, and destruction domains that are required for biological activity
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Loss of Geminin induces rereplication in the presence of functional p53
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Genotoxic stress leads to centrosome amplification in breast cancer cell lines that have an inactive G1/S cell cycle checkpoint
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Cdt1 phosphorylation by cyclin A-dependent kinases negatively regulates its function without affecting geminin binding
N Sugimoto et al.
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Centrosome aberrations: Cause or consequence of cancer progression?
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Mouse geminin inhibits not only Cdt1-MCM6 interactions but also a novel intrinsic Cdt1 DNA binding activity
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Cytoplasmic dynein/dynactin drives kinetochore protein transport to the spindle poles and has a role in mitotic spindle checkpoint inactivation
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The human licensing factor for DNA replication Cdt1 accumulates in G1 and is destabilized after initiation of S-phase
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It takes two to tango: understanding how centrosome duplication is regulated throughout the cell cycle
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Inhibition of eukaryotic DNA replication by geminin binding to Cdt1
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Formation of spindle poles by dynein/dynactin-dependent transport of NuMA
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