ArticleScientific reports2017
Pre-RC Protein MCM7 depletion promotes mitotic exit by Inhibiting CDK1 activity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- MCM7 supports the stemness of bladder cancer stem-like cells by enhancing autophagic flux.iScience · 2022Article
- Developmental lineage of human pluripotent stem cell-derived cardiac fibroblasts affects their functional phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Interactome of the Autoimmune Risk Protein ANKRD55.Frontiers in immunology · 2019Article
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MCM7, a subunit of mini-chromosome maintenance proteins (MCM) complex, plays an important role in initiating DNA replication during the G1 phase and extending DNA strands during the S phase. Here, we demonstrated that MCM7 is not only sustained but maintains association with chromatin during M phase. Remarkably, MCM7 siRNA can accelerate mitotic exit. MCM7 depletion leads to CDK1 inactivation and promotes subsequent cohesin/RAD21 cleavage, which eventually leads to sister chromatin segregation. Moreover, MCM7 is co-localized with tubulin in the mitotic cells and MCM7 depletion results in aberrant mitosis. Our results indicate that MCM7 may exert certain functions on spindle formation to prevent cytokinesis during early mitosis by regulating CDK1 activity.
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