ArticleNucleic acids research2012
Post-transcriptional homeostasis and regulation of MCM2-7 in mammalian cells.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 45 citations in OpenAlex.
- Combining single cell and bulk transcriptomics with Mendelian randomization identifies gut microbiota related prognostic genes and mechanisms in thyroid cancer.Discover oncology · 2026Article
- Chronic replication stress-mediated genomic instability disrupts placenta development in mice.PLoS genetics · 2026Article
- SETD3-mediated histidine methylation of MCM7 regulates DNA replication by facilitating chromatin loading of MCM.Science China. Life sciences · 2025Article
- Aggressive Serous Carcinomas of the Female Reproductive Tract: Cancer-Prone Cell States and Genetic Drivers.Cancers · 2025Review
- Gene choice in cancer cells is exclusive in ion transport but concurrent in DNA replication.Computational and structural biotechnology journal · 2024Article
- Multi-omics pan-cancer analyses identify MCM4 as a promising prognostic and diagnostic biomarker.Scientific reports · 2024Article
- Essential role of CK2α for the interaction and stability of replication fork factors during DNA synthesis and activation of the S-phase checkpoint.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Systemic Analysis of the DNA Replication Regulator MCM Complex in Ovarian Cancer and Its Prognostic Value.Frontiers in oncology · 2021Article
- Diagnostic and prognostic value of MCM3 and its interacting proteins in hepatocellular carcinoma.Oncology letters · 2020Article
- Article
- Recent trends in predictive biomarkers for determining malignant potential of oral potentially malignant disorders.Oncology reviews · 2019Article
- Article
- Resting cells rely on the DNA helicase component MCM2 to build cilia.Nucleic acids research · 2019Article
- O-GlcNAc transferase associates with the MCM2-7 complex and its silencing destabilizes MCM-MCM interactions.Cellular and molecular life sciences : CMLS · 2018Article
- Article
- ADAM10 and γ-secretase regulate sensory regeneration in the avian vestibular organs.Developmental biology · 2017Article
- Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth.Cell death & disease · 2017Article
- Too much to handle - how gaining chromosomes destabilizes the genome.Cell cycle (Georgetown, Tex.) · 2016Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The MiniChromosome Maintenance 2-7 (MCM2-7) complex provides essential replicative helicase function. Insufficient MCMs impair the cell cycle and cause genomic instability (GIN), leading to cancer and developmental defects in mice. Remarkably, depletion or mutation of one Mcm can decrease all Mcm levels. Here, we use mice and cells bearing a GIN-causing hypomophic allele of Mcm4 (Chaos3), in conjunction with disruption alleles of other Mcms, to reveal two new mechanisms that regulate MCM protein levels and pre-RC formation. First, the Mcm4(Chaos3) allele, which disrupts MCM4:MCM6 interaction, triggers a Dicer1 and Drosha-dependent ≈ 40% reduction in Mcm2-7 mRNAs. The decreases in Mcm mRNAs coincide with up-regulation of the miR-34 family of microRNAs, which is known to be Trp53-regulated and target Mcms. Second, MCM3 acts as a negative regulator of the MCM2-7 helicase in vivo by complexing with MCM5 in a manner dependent upon a nuclear-export signal-like domain, blocking the recruitment of MCMs onto chromatin. Therefore, the stoichiometry of MCM components and their localization is controlled post-transcriptionally at both the mRNA and protein levels. Alterations to these pathways cause significant defects in cell growth reflected by disease phenotypes in mice.
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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.