ArticleThe Journal of biological chemistry2013
Phosphorylation of minichromosome maintenance protein 7 (MCM7) by cyclin/cyclin-dependent kinase affects its function in cell cycle regulation.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Ribonucleotide reductase M1 regulates the cell cycle via minichromosome maintenance proteins.Genes & diseases · 2026Article
- Prognostic and Clinical Significance of the Proliferation Marker MCM7 in Breast Cancer.Pathobiology : journal of immunopathology, molecular and cellular biology · 2025Article
- The Low Tumorigenic Risk and Subtypes of Cardiomyocytes Derived from Human-induced Pluripotent Stem Cells.Current stem cell research & therapy · 2025Article
- Review
- Hypoxic reactivation of Kaposi's sarcoma associated herpesvirus.Cell insight · 2024Review
- Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence.Biomolecules · 2023Review
- Early diagnostic and prognostic biomarkers for gastric cancer: systems-level molecular basis of subsequent alterations in gastric mucosa from chronic atrophic gastritis to gastric cancer.Journal, genetic engineering & biotechnology · 2023Article
- Comprehensive analysis of the correlation of the pan-cancer gene HAUS5 with prognosis and immune infiltration in liver cancer.Scientific reports · 2023Article
- Review
- Review
- Quantitative profiling of adaptation to cyclin E overproduction.Life science alliance · 2022Article
- Article
- Elevated expression of minichromosome maintenance 3 indicates poor outcomes and promotes G1/S cell cycle progression, proliferation, migration and invasion in colorectal cancer.Bioscience reports · 2020Article
- Post-Translational Modifications of the Mini-Chromosome Maintenance Proteins in DNA Replication.Genes · 2019Review
- Nuclear Prohibitin3 Maintains Genome Integrity and Cell Proliferation in the Root Meristem through Minichromosome Maintenance 2.Plant physiology · 2019Article
- O-GlcNAc transferase associates with the MCM2-7 complex and its silencing destabilizes MCM-MCM interactions.Cellular and molecular life sciences : CMLS · 2018Article
- The Expression of MCM7 is a Useful Biomarker in the Early Diagnostic of Gastric Cancer.Pathology oncology research : POR · 2018Article
- Role of MCM2-7 protein phosphorylation in human cancer cells.Cell & bioscience · 2018Review
- Sub-minute Phosphoregulation of Cell Cycle Systems during Plasmodium Gamete Formation.Cell reports · 2017Article
- Article
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5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MCM7 is one of the subunits of the MCM2-7 complex that plays a critical role in DNA replication initiation and cell proliferation of eukaryotic cells. After forming the pre-replication complex (pre-RC) with other components, the MCM2-7 complex is activated by DDK/cyclin-dependent kinase to initiate DNA replication. Each subunit of the MCM2-7 complex functions differently under regulation of various kinases on the specific site, which needs to be investigated in detail. In this study, we demonstrated that MCM7 is a substrate of cyclin E/Cdk2 and can be phosphorylated on Ser-121. We found that the distribution of MCM7-S121A is different from wild-type MCM7 and that the MCM7-S121A mutant is much less efficient to form a pre-RC complex with MCM3/MCM5/cdc45 compared with wild-type MCM7. By using the Tet-On inducible HeLa cell line, we revealed that overexpression of wild-type MCM7 but not MCM7-S121A can block S phase entry, suggesting that an excess of the pre-RC complex may activate the cell cycle checkpoint. Further analysis indicates that the Chk1 pathway is activated in MCM7-overexpressed cells in a p53-dependent manner. We performed experiments with the human normal cell line HL-7702 and also observed that overexpression of MCM7 can cause S phase block through checkpoint activation. In addition, we found that MCM7 could also be phosphorylated by cyclin B/Cdk1 on Ser-121 both in vitro and in vivo. Furthermore, overexpression of MCM7-S121A causes an obvious M phase exit delay, which suggests that phosphorylation of MCM7 on Ser-121 in M phase is very important for a proper mitotic exit. These data suggest that the phosphorylation of MCM7 on Ser-121 by cyclin/Cdks is involved in preventing DNA rereplication as well as in regulation of the mitotic exit.
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