ArticleFEBS open bio2026
Overexpression of CDT1 inhibits cell cycle progression at S phase by interacting with the mini-chromosome maintenance complex and causes DNA damage.
Article in FEBS open bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- CDT1 acts with the replisome to remodel replication forks.Science advances · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Cdc10-dependent transcript 1 (CDT1) is an essential protein for DNA replication licensing, which loads the mini-chromosome maintenance (MCM) complex onto replication origins. We previously reported that excess CDT1 inhibits the elongation of nascent strands during DNA replication in Xenopus egg extracts. In the present study, we investigated the underlying mechanism through which CDT1 inhibits replication fork progression by expressing various CDT1 mutants in human cells. Initiation of DNA replication resulted in downregulation of CDT1, preventing MCM reloading within the same cell cycle; thus, CDT1 overexpression induces rereplication. In this study, we observed that overexpression of a mutant CDT1 lacking licensing activity induced cell cycle arrest at the S phase in human cells. An additional mutation in the MCM-binding domain reduced this cell cycle inhibitory effect. Furthermore, overexpression of CDT1 induced DNA damage independent of its licensing activity. These results suggest that CDT1 overexpression inhibits the progression of replication forks by interacting with the MCM complex, leading to the stalling and collapse of replication forks.
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