ArticleProceedings of the National Academy of Sciences of the United States of America2009
Quaternary structure of the human Cdt1-Geminin complex regulates DNA replication licensing.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 81 citations in OpenAlex.
- Novel heterozygous GMNN variants in human early embryonic arrest involving CHK1‑mediated cell cycle dysregulation.Journal of assisted reproduction and genetics · 2026Article
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- 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
- Geminin inhibits DNA replication licensing by sterically blocking CDT1-MCM2 interactions.Nature communications · 2025Article
- SEC-SAXS/MC Ensemble Structural Studies of the Microtubule Binding Protein Cdt1 Show Monomeric, Folded-Over Conformations.Cytoskeleton (Hoboken, N.J.) · 2025Article
- The Crk4-Cyc4 complex regulates GThe EMBO journal · 2024Article
- SAXS/MC studies of the mixed-folded protein Cdt1 reveal monomeric, folded over conformations.bioRxiv : the preprint server for biology · 2024Article
- CDT1 inhibits CMG helicase in early S phase to separate origin licensing from DNA synthesis.Molecular cell · 2023Article
- Small Molecule Inhibitor Targeting CDT1/Geminin Protein Complex Promotes DNA Damage and Cell Death in Cancer Cells.Frontiers in pharmacology · 2022Article
- SPOP mutation induces replication over-firing by impairing Geminin ubiquitination and triggers replication catastrophe upon ATR inhibition.Nature communications · 2021Article
- Replication initiation: Implications in genome integrity.DNA repair · 2021Review
- The DNA binding domain of the Vibrio vulnificus SmcR transcription factor is flexible and binds diverse DNA sequences.Nucleic acids research · 2021Article
- Regulation of DNA Replication Licensing and Re-Replication by Cdt1.International journal of molecular sciences · 2021Review
- SIX3 and SIX6 interact with GEMININ via C-terminal regions.Biochemistry and biophysics reports · 2019Article
- Article
- Mathematical modelling reveals unexpected inheritance and variability patterns of cell cycle parameters in mammalian cells.PLoS computational biology · 2019Article
- Cdt1 variants reveal unanticipated aspects of interactions with cyclin/CDK and MCM important for normal genome replication.Molecular biology of the cell · 2018Article
- Cdt1 stabilizes kinetochore-microtubule attachments via an Aurora B kinase-dependent mechanism.The Journal of cell biology · 2018Article
- Review
- Controlling centriole numbers: Geminin family members as master regulators of centriole amplification and multiciliogenesis.Chromosoma · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
All organisms need to ensure that no DNA segments are rereplicated in a single cell cycle. Eukaryotes achieve this through a process called origin licensing, which involves tight spatiotemporal control of the assembly of prereplicative complexes (pre-RCs) onto chromatin. Cdt1 is a key component and crucial regulator of pre-RC assembly. In higher eukaryotes, timely inhibition of Cdt1 by Geminin is essential to prevent DNA rereplication. Here, we address the mechanism of DNA licensing inhibition by Geminin, by combining X-ray crystallography, small-angle X-ray scattering, and functional studies in Xenopus and mammalian cells. Our findings show that the Cdt1:Geminin complex can exist in two distinct forms, a "permissive" heterotrimer and an "inhibitory" heterohexamer. Specific Cdt1 residues, buried in the heterohexamer, are important for licensing. We postulate that the transition between the heterotrimer and the heterohexamer represents a molecular switch between licensing-competent and licensing-defective states.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.