ArticleThe Journal of cell biology2011
Highly stable loading of Mcm proteins onto chromatin in living cells requires replication to unload.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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
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.
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Who cites it
61 citing papers in PubMed, 92 citations in OpenAlex.
- Distinct roles of MCM2-7 subunits in replication licensing in human cells.Nature communications · 2026Article
- Transcription elongation can be sufficient, but is not necessary, to advance replication timing.EMBO reports · 2026Article
- DNA replication fork speed acts as a pacer in cortical neurogenesis.Nature communications · 2025Article
- Temporal control of human DNA replication licensing by CDK4/6-RB signalling and chemical genetics.Nature communications · 2025Article
- Transcription can be sufficient, but is not necessary, to advance replication timing.bioRxiv : the preprint server for biology · 2025Article
- Characterizing replisome disassembly in human cells.iScience · 2024Article
- Unwinding Helicase MCM Functionality for Diagnosis and Therapeutics of Replication Abnormalities Associated with Cancer: A Review.Molecular diagnosis & therapy · 2024Review
- Quantity and quality of minichromosome maintenance protein complexes couple replication licensing to genome integrity.Communications biology · 2024Review
- Replication licensing during S phase: breaking the law to prevent breaking DNA.Nature structural & molecular biology · 2023Article
- Promitotic Action ofInternational journal of molecular sciences · 2022Article
- Solving the MCM paradox by visualizing the scaffold of CMG helicase at active replisomes.Nature communications · 2022Article
- The consequences of differential origin licensing dynamics in distinct chromatin environments.Nucleic acids research · 2022Article
- You shall not pass! Unveiling the barriers for cohesin-mediated loop extrusion.Molecular cell · 2022Article
- Article
- Chromatin loading of MCM hexamers is associated with di-/tri-methylation of histone H4K20 toward S phase entry.Nucleic acids research · 2021Article
- The H3.3K27M oncohistone affects replication stress outcome and provokes genomic instability in pediatric glioma.PLoS genetics · 2021Article
- Efficiency and equity in origin licensing to ensure complete DNA replication.Biochemical Society transactions · 2021Review
- Mammalian DNA Replication Timing.Cold Spring Harbor perspectives in biology · 2021Review
- Article
- Chromatin and Nuclear Dynamics in the Maintenance of Replication Fork Integrity.Frontiers in genetics · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The heterohexameric minichromosome maintenance protein complex (Mcm2-7) functions as the eukaryotic helicase during DNA replication. Mcm2-7 loads onto chromatin during early G1 phase but is not converted into an active helicase until much later during S phase. Hence, inactive Mcm complexes are presumed to remain stably bound from early G1 through the completion of S phase. Here, we investigated Mcm protein dynamics in live mammalian cells. We demonstrate that Mcm proteins are irreversibly loaded onto chromatin cumulatively throughout G1 phase, showing no detectable exchange with a gradually diminishing soluble pool. Eviction of Mcm requires replication; during replication arrest, Mcm proteins remained bound indefinitely. Moreover, the density of immobile Mcms is reduced together with chromatin decondensation within sites of active replication, which provides an explanation for the lack of colocalization of Mcm with replication fork proteins. These results provide in vivo evidence for an exceptionally stable lockdown mechanism to retain all loaded Mcm proteins on chromatin throughout prolonged cell cycles.
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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.