ReviewMolecular biology international2014
MCM Paradox: Abundance of Eukaryotic Replicative Helicases and Genomic Integrity.
Review in Molecular biology international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed.
- MCM2-7 proteins promote NF-κB transcriptional activity through cooperative promoter recruitment.Bioscience reports · 2026Article
- TMT-based quantitative proteomic assessment of Vicia sativa induced neurotoxicity by β-cyano-L-alanine and γ-glutamyl-β-cyano-L-alanine in SH-SY5Y cells.Scientific reports · 2025Article
- Regulation of replication timing in Saccharomyces cerevisiae.PLoS computational biology · 2025Article
- Identification of MCM2-Interacting Proteins Associated with Replication Initiation Using APEX2-Based Proximity Labeling Technology.International journal of molecular sciences · 2025Article
- Review
- Case Report: Molecular Analyses of Cell-Cycle-Related Genes in Cortical Brain Tissue of a Patient with Rasmussen Encephalitis.International journal of molecular sciences · 2024Article
- Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response.Nature communications · 2024Article
- Comparative proteomics analysis of the mouse mini-gut organoid: insights into markers of gluten challenge from celiac disease intestinal biopsies.Frontiers in molecular biosciences · 2024Article
- Unwinding the Role of the CMG Helicase in Inborn Errors of Immunity.Journal of clinical immunology · 2023Article
- Review
- Partial loss-of-function mutations in GINS4 lead to NK cell deficiency with neutropenia.JCI insight · 2022Article
- MCM7 supports the stemness of bladder cancer stem-like cells by enhancing autophagic flux.iScience · 2022Article
- Nucleosome-directed replication origin licensing independent of a consensus DNA sequence.Nature communications · 2022Article
- Selective role of the DNA helicase Mcm5 in BMP retrograde signaling during Drosophila neuronal differentiation.PLoS genetics · 2022Article
- Article
- A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.PLoS biology · 2022Article
- The H3.3K27M oncohistone affects replication stress outcome and provokes genomic instability in pediatric glioma.PLoS genetics · 2021Article
- Genomic analysis finds no evidence of canonical eukaryotic DNA processing complexes in a free-living protist.Nature communications · 2021Article
- MCM-2, Ki-67, and EGFR downregulated expression levels in advanced stage laryngeal squamous cell carcinoma.Scientific reports · 2021Article
- Plasma membrane calcium ATPase 1 regulates human umbilical vein endothelial cell angiogenesis and viability.Journal of molecular and cellular cardiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a crucial component of DNA replication licensing system, minichromosome maintenance (MCM) 2-7 complex acts as the eukaryotic DNA replicative helicase. The six related MCM proteins form a heterohexamer and bind with ORC, CDC6, and Cdt1 to form the prereplication complex. Although the MCMs are well known as replicative helicases, their overabundance and distribution patterns on chromatin present a paradox called the "MCM paradox." Several approaches had been taken to solve the MCM paradox and describe the purpose of excess MCMs distributed beyond the replication origins. Alternative functions of these MCMs rather than a helicase had also been proposed. This review focuses on several models and concepts generated to solve the MCM paradox coinciding with their helicase function and provides insight into the concept that excess MCMs are meant for licensing dormant origins as a backup during replication stress. Finally, we extend our view towards the effect of alteration of MCM level. Though an excess MCM constituent is needed for normal cells to withstand stress, there must be a delineation of the threshold level in normal and malignant cells. This review also outlooks the future prospects to better understand the MCM biology.
Identifiers
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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.